bims-carter Biomed News
on CAR-T Therapies
Issue of 2026–01–04
thirty-one papers selected by
Luca Bolliger, lxBio



  1. Front Immunol. 2025 ;16 1701655
      Cellular senescence is a complex biological process that contributes to the progression of age-related diseases. Senescent cells accumulate over time and secrete proinflammatory factors that disrupt tissue homeostasis and promote chronic diseases. Initially created for cancer immunotherapy, chimeric antigen receptor (CAR) T cell therapy has recently been repurposed at the preclinical level to eliminate senescent cells by recognizing senescence-associated surface markers. Recent preclinical studies have demonstrated the feasibility of anti-uPAR and anti-NKG2D CAR T cell-based approaches for eliminating senescent cells in preclinical models of fibrosis, metabolic disorders, and natural aging, resulting in reduced fibrotic burden, improved metabolic parameters, and enhanced tissue function. However, several challenges remain in their clinical applicability, including the identification of specific and universal senescence markers, potential off-target effects, and long-term safety concerns. Additionally, immunosenescence, an age-related decline in immune function, poses challenges for CAR T cell therapy in elderly patients. This review discusses recent advancements in CAR T cell therapy for senescence clearance, highlighting key molecular targets, preclinical findings, and future research directions. Despite their promise, a significant translational gap persists, and further research is required to improve the specificity, efficacy, and readiness for future human clinical trials.
    Keywords:  CAR T cell; aging-related diseases; immunotherapy; senescence; targeting senescent cells
    DOI:  https://doi.org/10.3389/fimmu.2025.1701655
  2. Int J Mol Sci. 2025 Dec 10. pii: 11898. [Epub ahead of print]26(24):
      Despite the groundbreaking impact of currently approved CAR T-cell therapies, substantial unmet clinical needs remain. This highlights the need for CAR T treatments that are easier to tune, combine, and program with logic rules, in oncology and autoimmunity. Modular CAR T cells use a two-part system: the CAR on the T cell binds an adaptor molecule (AM), and that adaptor binds the tumour-associated antigen (TAA). This design separates recognition of the target antigen and activation of the T cells, resulting in a cellular therapy concept with better control, flexibility, and safety compared to established direct-targeting CAR T-cell systems. The key advantage of the system is the adaptor molecule, often an antibody-based reagent, that targets the TAA. Adaptors can be swapped or combined without re-engineering the T cells, enabling straightforward multiplexing and logic-gated control. The CAR itself is designed to recognise the AM via a unique tag on the adaptor. Only when the CAR, AM, and antigen-positive target cell assemble correctly is T-cell effector function activated, leading to cancer cell lysis. This two-component system has several features that need to be considered when designing a modular CAR: First, the architecture of the CAR, i.e., how the binding domain and the backbone are designed, can influence tonic signalling and activation/exhaustion parameters. Second, the affinity of CAR-AM and AM-TAA will mostly define the engagement kinetics of the system. Third, the valency of the AM has an impact on exhaustion and non-specific activation of CAR T cells. And lastly, the architecture of the AM, especially the size, defines the pharmacokinetics and, consequently, the dosing scheme of the AM. The research conducted on direct-targeting CAR T cells have generated in-depth knowledge of the advantages and disadvantages of the technology in its current form, with remarkable clinical success in relapsed/refractory disease and long-term survival in otherwise difficult-to-treat patient populations. On the other hand, CAR T-cell therapy poses the risk of severe adverse events and antigen loss coupled with antigen-negative relapse which remains the main reason for failed therapies. Addressing these issues in the traditional setting of one CAR targeting one antigen will always be difficult due to the heterogeneous nature of most oncologic diseases, but the flexibility to change target antigens and the modulation of CAR T response by dosing the AM in a modular CAR system might be pivotal to mitigate these hurdles of direct CAR T cells. Since the first conception of modular CARs in 2012, there have been more than 30 constructs published, and some of those have been translated into phase I/II clinical trials with early signs of success, but whether these will progress into a late-stage clinical trial and gain regulatory approval remains to be seen.
    Keywords:  CAR T cell; adaptor CAR; adaptor molecule (AM); antigen receptor; indirect CAR; modular CAR; switchable CAR
    DOI:  https://doi.org/10.3390/ijms262411898
  3. J Clin Invest. 2026 Jan 02. pii: e201161. [Epub ahead of print]136(1):
      Chimeric antigen receptor T cell (CAR-T) therapy has transformed the treatment of hematologic malignancies, yet, severe inflammatory toxicities continue to limit its broader use. In this issue of the JCI, Goala et al. uncovered a mechanistic link between IFN-γ-driven inflammation and disrupted neutrophil homeostasis, revealing that cytokine release syndrome (CRS) and immune cell-associated hematologic toxicity (ICAHT) stem from a shared biological pathway. Using IL-2Ra-deficient mice and patient samples, they showed that IFN-γ suppressed IL-17A and granulocyte colony-stimulating factor (G-CSF), disrupting granulopoiesis and neutrophil survival. Strikingly, IFN-γ blockade eased both CRS and neutropenia without diminishing CAR-T efficacy, suggesting a path toward safer, better-tolerated cell therapies.
    DOI:  https://doi.org/10.1172/JCI201161
  4. Curr Microbiol. 2025 Dec 27. 83(2): 106
      Chimeric antigen receptor (CAR)-based immunotherapies face significant translational challenges in solid tumor applications, particularly regarding manufacturing scalability, tumor targeting specificity, and antigen heterogeneity. This systematic review evaluates microbial systems as innovative platforms to address these limitations through synthetic biology-driven approaches, with a focus on bridging preclinical advances to clinical implementation. Analysis of 389 peer-reviewed studies (2015-2025) reveals that engineered probiotic strains (e.g., Escherichia coli Nissle 1917) achieve selective tumor colonization while functioning as programmable factories for:1. Synthetic antigen production and single-chain variable fragment (scFv) expression,2. Costimulatory domain delivery enabling antigen-agnostic CAR-T activation,3. Tumor microenvironment modulation via immunostimulatory chemokines. Microbial platforms demonstrate superior manufacturing economics (70-90% cost reduction vs. conventional methods) and enhance CAR-T functionality through epigenetic reprogramming by microbial metabolites (e.g., short-chain fatty acids). CRISPR/Cas-engineered genetic circuits further enable precise spatiotemporal control of therapeutic payloads.Microbial systems represent transformative platforms for scalable, programmable CAR immunotherapy with significant potential for solid tumor targeting. Key barriers to clinical translation include biocontainment challenges, incomplete mechanistic understanding of tumor homing specificity, and safety validation requirements. Strategic integration of synthetic biology with microbial chassis offers a viable pathway toward accessible next-generation cancer therapies.
    Keywords:  CAR-based therapies (or Chimeric antigen receptor therapy); Cancer immunotherapy; Engineered probiotics; Microbial systems; Synthetic biology; Translational immunotherapy; Tumor homing mechanisms
    DOI:  https://doi.org/10.1007/s00284-025-04679-z
  5. Biology (Basel). 2025 Dec 15. pii: 1790. [Epub ahead of print]14(12):
      Chimeric antigen receptor (CAR)-T cell therapies represent a promising therapeutic approach for refractory autoimmune diseases. Although autologous CAR-T cells have achieved success thus far, they require expensive, individualised manufacturing, limiting their commercialisation potential. Allogeneic alternatives could overcome these scalability barriers, providing 'off-the-shelf' treatments, although they raise the issues of graft-vs-host reactions and host-mediated rejection. To mitigate such risks, gene-edited αβ T cells or non-alloreactive host cells (e.g., NK cells, γδ T cells) may be used. This review evaluates evidence of the functionality and commercial potential of various allogeneic CAR-T solutions for autoimmunity. Searches were conducted of PubMed, EMBASE and Web of Science to extract clinical and preclinical studies of allogeneic CAR-T cells, for the treatment of autoimmune diseases and B or T cell malignancies. In light of the paucity of data on autoimmune disease, the latter were included to facilitate extrapolation to the autoimmune setting. A total of 107 studies were included. The available clinical outcomes of efficacy and safety, as well as preclinical key findings, are reported. Current developments and potential future improvements for safety, effectiveness and cost-effective manufacture are then discussed. The findings of this review demonstrate the promising therapeutic potential of allogeneic CAR-T for autoimmune disease, with scope for the further optimisation of safety and scalable manufacture to facilitate commercialisation.
    Keywords:  CAR-T cell; allogeneic; autoimmune disease; chimeric antigen receptor; off the shelf
    DOI:  https://doi.org/10.3390/biology14121790
  6. Methods Mol Biol. 2026 ;2983 257-264
      Chimeric antigen receptor T cells (CAR T cells) therapy has revolutionarily changed the landscape of immunotherapy and been approved by the U. S Food and Drug Administration (FDA) since 2017 for several blood malignancies. To translate novel CAR T cells into clinical applications, it is essential to evaluate their antigen specificity, cytotoxic capacity, and off-target effects in vitro. A commonly used criteria to assess CAR T cell functionality involves detecting cytokine secretion following their engagement with target antigens. This chapter describes a method of combining intracellular cytokine staining and multi-color flow cytometry to measure CAR T cells activation following antigen stimulation.
    Keywords:  CAR T cells; Chimeric antigen receptor T cells; Flow cytometry; Immunotherapy; Intracellular cytokine staining; T cell activation
    DOI:  https://doi.org/10.1007/978-1-0716-4901-5_22
  7. J Am Chem Soc. 2026 Jan 02.
      The clinical application of chimeric antigen receptor (CAR) T cell therapy in solid tumors remains limited due to significant safety concerns, particularly "on-target, off-tumor" toxicity and cytokine release syndrome (CRS). Here, we describe a class of CARs that employ disulfide-directed multicyclic peptides (DDMPs) as compact antigen-recognition domains targeting the tumor-associated antigens HER2 and TROP2. DDMP-based CAR T cells exhibited antigen density-dependent cytotoxicity in vitro and in vivo, efficiently eliminating cells with high antigen expression while sparing cells with low antigen levels, thereby mitigating on-target, off-tumor toxicity. In addition, DDMP-based CAR T cells secreted markedly lower levels of pro-inflammatory cytokines upon targeted killing, reducing CRS risk. Mechanistic analyses revealed that this favorable combination of restrained cytokine release and density-gated killing is associated with distinct T cell signaling pathway engagement and reduced cell avidity relative to conventional single-chain variable fragment (scFv)-based CAR T cells. Collectively, these findings establish DDMP-based CARs as a promising framework for engineering safer, yet efficacious, CAR T therapies for solid tumors.
    DOI:  https://doi.org/10.1021/jacs.5c13642
  8. Viruses. 2025 Dec 14. pii: 1615. [Epub ahead of print]17(12):
      Antiretroviral therapy (ART) effectively suppresses HIV replication but fails to eradicate latent reservoirs, leading to viral rebound after interruption. Chimeric antigen receptor (CAR) T-cell therapy offers a potential strategy to achieve durable remission. A systematic PubMed search (July 2020-June 2025) identified 253 studies on CAR-T therapy in HIV; 74 met inclusion criteria and were qualitatively analyzed. Preclinical data showed that CAR-T cells can recognize and eliminate infected cells, reach viral reservoirs, and persist long term, particularly when derived from hematopoietic stem cells. Dual-target and combination approaches with checkpoint inhibitors or latency-reversing agents enhanced antiviral efficacy. Early clinical studies confirmed safety and modest reservoir reduction. CAR-T cell therapy represents a promising step toward a functional HIV cure. Further optimization of design, integration with gene-editing technologies, and standardized clinical evaluation are required to confirm durable efficacy and safety.
    Keywords:  CAR-T cells; HIV cure; gene editing
    DOI:  https://doi.org/10.3390/v17121615
  9. Stem Cell Rev Rep. 2025 Dec 27.
      Ovarian cancer (OC) remains the deadliest gynecological malignancy, characterized by late diagnosis, tumor heterogeneity, and chemotherapy resistance, contributing to poor survival rates. This comprehensive review explores the potential of chimeric antigen receptor (CAR)-T and CAR-natural killer (NK) cell therapies as emerging immunotherapies for OC. We examine key tumor-associated antigens, including folate receptor alpha (FRα), mesothelin (MSLN), HER2, EpCAM, MUC16, Tn-glycopeptide, TAG-72, and LGR5, which are overexpressed in OC and have shown promise in preclinical studies and early clinical trials for inducing tumor regression without MHC restrictions. While CAR-T cells have demonstrated significant antitumor cytotoxicity in preclinical models, their application in solid tumors like OC faces challenges, including immunosuppressive tumor microenvironments, antigen escape, cytokine release syndrome, and neurotoxicity. CAR-NK cells offer potential advantages, such as reduced toxicity, off-the-shelf availability, and efficacy against heterogeneous tumors, making them a promising complementary approach. This review discusses current research on dosing regimens and combination strategies involving checkpoint inhibitors, chemotherapy, and radiotherapy, as well as responses across histological subtypes. Drawing from ongoing early-phase trials and innovative approaches like CRISPR editing and dual-targeting, we highlight the progress and challenges in developing CAR-based therapies, underscoring their potential while emphasizing the need for further research to establish clinical efficacy in OC.
    Keywords:  CAR; CAR-NK cell; CAR-T cell; Combination therapy; Ovarian cancer; Tumor microenvironment
    DOI:  https://doi.org/10.1007/s12015-025-11024-1
  10. J Neuroinflammation. 2025 Dec 30.
    ECF Young Investigators/Fellows Initiative
      Chimeric antigen receptor (CAR) T-cell therapy is rapidly emerging as a transformative approach for treating multiple sclerosis (MS) and other neuroimmune disorders such as neuromyelitis optica spectrum disorder (NMOSD), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and myasthenia gravis (MG), alongside several other rare neuroimmunological conditions currently being evaluated in compassionate-use or early-phase studies. These conditions are driven in part by autoreactive B cells that sustain chronic inflammation and progressive tissue damage. While current immunomodulatory therapies have improved clinical outcomes, they often require lifelong administration and fail to effectively eliminate compartmentalized inflammation within the central nervous system. Recent advances in CD19- and BCMA-directed CAR T-cell therapy, initially developed for hematologic malignancies, demonstrate the potential to achieve targeted, durable B-cell depletion and immune reprogramming in autoimmune diseases. Preclinical models and early-phase clinical trials have shown promising efficacy, including reduced relapse rates, stabilization of disability progression, and decreased autoantibody levels, alongside a favorable safety profile with lower rates of high-grade cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) compared to oncologic applications. This review synthesizes the current evidence supporting the use of CAR T-cell therapy in neuroinflammatory diseases and explores its potential to redefine treatment paradigms by shifting from chronic immunosuppression to long-term immune tolerance, creating a favorable environment for repair mechanisms. Realizing the full therapeutic promise of CAR T-cells in autoimmune neurology will require sustained research in heterogeneous populations and across disease spectrums.
    Keywords:  Autoimmune disorders; Autoimmune neurology; B cells; Chimeric antigen receptor t cells; Immunotherapy; Multiple sclerosis; Neuroinflammation
    DOI:  https://doi.org/10.1186/s12974-025-03668-0
  11. J Exp Med. 2026 Feb 02. pii: e20251652. [Epub ahead of print]223(2):
      T cell engagers (TCEs) are antibody-based constructs designed to transiently reprogram cytotoxic T lymphocytes for target cell elimination by simultaneously binding the T cell receptor and a specific surface antigen on the target cell. Over the past 12 years, 10 TCEs were approved by the US Food and Drug Administration, and an additional two by the European Medicines Agency. Nine TCEs treat hematologic malignancies, and three target solid tumors. Over 150 TCEs are being investigated in clinical trials, recently also in autoimmune diseases. Here, we discuss the learnings from the 12 approved TCEs. A surprising variety of molecular designs and biochemical characteristics appear suitable for approval. On the clinical side, we review targets, indications, dosing, schedules, side effects, mitigation strategies for adverse events, and efficacy. High flexibility in design and choice of target, scalability, high response rates as a monotherapy in hematologic malignancies, and emerging efficacy against solid tumors and in autoimmune diseases make TCEs an attractive therapeutic modality.
    DOI:  https://doi.org/10.1084/jem.20251652
  12. Immunother Adv. 2026 ;6(1): ltaf036
      T cell (Tc) receptor (TCR)-based cell therapies have shown clinical efficacy across many cancer types and represent an attractive strategy for targeting solid tumors. However, the immunosuppressive tumor microenvironment, downregulation of target antigen and HLA, and the need for an autologous source limit the efficacy and the accessibility of TCR-Tc therapies. Early clinical trials have shown the potential of natural killer cells (NKs) as a therapy to treat hematological and solid cancers. Allogeneic NKs, engineered to express a TCR, represent a novel and promising strategy overcoming the limitations of T and NKs therapies. Here we describe the development of a product consisting of NKs engineered to express an affinity-enhanced TCR recognizing MAGE-A4, a clinically validated tumor antigen expressed across several solid tumors. The introduction of the TCR does not disrupt the innate functionality of NKs and adds TCR-mediated specific killing of antigen-positive targets. In fact, the innate potential of the NKs appears to be enhanced by the presence of the CD3-TCR complex, creating NKs with increased potency. TCR-NKs are faster, more potent than TCR-Tc and retain killing activity in the absence of TCR target antigen thus potentially overcoming tumor heterogeneity and/or antigen loss. Lastly, TCR-NKs are not activated when co-cultured with normal cells, displaying a safe profile. Combining the innate cytotoxicity of NKs with MAGE-A4-specific targeting of an affinity-enhanced TCR, results in a potent and safe cellular product representing a promising and novel therapeutic off-the-shelf paradigm for the treatment of many solid cancers.
    Keywords:  MAGE-A4; TCR-NK cells; affinity enhancement; immunotherapy; solid tumors
    DOI:  https://doi.org/10.1093/immadv/ltaf036
  13. Pharmaceutics. 2025 Nov 26. pii: 1520. [Epub ahead of print]17(12):
      Background/Objectives: Chimeric antigen receptor (CAR) T cells have shown remarkable clinical success in certain blood cancers but remain largely ineffective in solid tumors. A major reason for this limitation is the hostile tumor microenvironment, which restricts oxygen and nutrients while producing toxic metabolites that suppress immune cell activity. This review aims to examine how targeted metabolic reprogramming can overcome these barriers and improve CAR T cell performance. Methods: We evaluated preclinical and translational studies that focused on engineering CAR T cells to resist hypoxia, improve nutrient utilization, reduce metabolic exhaustion, and counteract suppressive metabolites in solid tumors. Results: Emerging strategies include engineering resistance to low oxygen and high lactate, enhancing nutrient uptake through transporter overexpression, and blocking inhibitory pathways such as those driven by adenosine. These approaches improve CAR T cell persistence, memory formation, and cytotoxic function in challenging tumor environments. Conclusions: Integrating metabolic reprogramming with conventional CAR design is essential to unlock the full potential of CAR T therapy against solid tumors. Continued innovation in this area will be critical for translating laboratory advances into effective clinical treatments.
    Keywords:  CAR T cells; adenosine; hypoxia; metabolic reprogramming; tumor microenvironment
    DOI:  https://doi.org/10.3390/pharmaceutics17121520
  14. Transplant Cell Ther. 2025 Dec 25. pii: S2666-6367(25)02649-1. [Epub ahead of print]
      Chimeric antigen receptor (CAR) T cell persistence with memory is the current research focus of cancer immunotherapy. The incomplete effect of CAR T cells against tumors results from CAR T cell dysfunction and exhaustion. Asymmetric cell division is an evolutionarily conserved mechanism to maintain mother stem cells during embryonic development, and for immune cells to provide a continuous supply of diverse populations to fight infections and cancer. CAR T cells use ACD to determine their fate during the first mitotic division after interaction with its target, creating a pool of memory CAR T cells which can be recalled to be effector cells during tumor relapse, necessarily to offset the diminished ability of exhausted CAR T cells in controlling the tumor. Affinity of the CAR T - target cell immune synapse and mitochondrial dynamics regulate ACD. We review the literature regarding CAR T cell persistence, exhaustion, and mechanisms of reversing exhaustion. Subsequently, we present a hypothesis linking mitophagy to CAR T cell exhaustion, modulation of which may be clinically relevant in the treatment of cancers with CAR T cells.
    Keywords:  Asymmetric cell division; CAR T cells; Exhaustion; Memory; Mitophagy; Persistence; T cells
    DOI:  https://doi.org/10.1016/j.jtct.2025.12.988
  15. Life (Basel). 2025 Dec 04. pii: 1862. [Epub ahead of print]15(12):
      Host-modulating therapies and oral microbiome-targeted approaches are emerging options in periodontal care and are especially relevant for patients undergoing immunotherapy for hematologic malignancies. Immune dysregulation induced by immune checkpoint inhibitors or CAR-T cell therapy may worsen periodontal inflammation and alter the composition and functions of the oral microbiota. Beyond these, other immunomodulatory treatments commonly employed in hematologic malignancies-including monoclonal antibodies (e.g., rituximab, daratumumab), immunomodulatory drugs (e.g., lenalidomide, thalidomide), cytokine-based therapies (e.g., interferon-α), and targeted small-molecule inhibitors (e.g., BTK inhibitors, JAK inhibitors) may also influence periodontal homeostasis and oral microbial ecology by altering neutrophil function, cytokine profiles, and mucosal immune surveillance. The oral microbiota is functionally connected with the intestinal microbial ecosystem through the oral-gut axis, by periodontal pathogens may colonize the gut and modulate systemic immune responses, with potential repercussions on the efficacy and safety of immunotherapy. This narrative review examines the mechanisms and clinical applicability of host-modulating therapies, including subantimicrobial-dose doxycycline, omega-3 fatty acids, and microbiome-targeted interventions, such as oral probiotics, prebiotics and other antimicrobials in patients treated with immunotherapy.
    Keywords:  anti-inflammatory agents; cancer immunotherapy; hematologic neoplasms; periodontal therapy; periodontitis; probiotics
    DOI:  https://doi.org/10.3390/life15121862
  16. Int J Mol Sci. 2025 Dec 11. pii: 11939. [Epub ahead of print]26(24):
      The thymus, as the primary lymphoid organ for T cell development, orchestrates a complex continuum of processes encompassing precursor migration, lymphocyte lineage commitment, and antigen-guided selection to generate a self-tolerant and immunocompetent T cell repertoire. The thymus is anatomically divided into the cortex, which facilitates the positive selection of thymocytes through interactions between T cell receptors and self-peptide-MHC complexes on cortical epithelial cells, and the medulla, which mediates negative selection by medullary epithelial cells in concert with dendritic cells via the presentation of self-antigens. Key regulatory elements controlling thymocyte development include the transcription factors ThPOK/Runx3 and Sox13/PLZF, chemokine-driven migration mediated by CXCR4 and CCR7, and cytokine signaling. These components collectively exert a profound influence on the final outcome: the establishment of TCR affinity thresholds for tissue-specific antigens in mature T cells. In summary, the integration of multidimensional methodologies highlights the pivotal role of the thymus in immune tolerance, with translational implications for autoimmunity, cancer immunotherapy, and regenerative medicine, as reviewed herein.
    Keywords:  T cells maturation; selection; thymus; thymus analysis; αβ T cells; γδ T cells
    DOI:  https://doi.org/10.3390/ijms262411939
  17. Cell Commun Signal. 2025 Dec 31.
      Solid tumors remain difficult to treat due to antigen heterogeneity, physical barriers that limit immune-cell trafficking, and a profoundly immunosuppressive tumor microenvironment (TME). Over the past decade, cancer immunotherapy advanced considerably through innovative strategies, including macrophage reprogramming and CAR-macrophages, dendritic-cell (DC) vaccines, natural killer (NK) and natural killer T (NKT) cell approaches, tumor-infiltrating lymphocyte (TIL) therapy, TCR-engineered and CAR-T cells, emerging B-cell engineering, and cell-derived extracellular vesicles (EVs). Here we summarize how each modality interacts with the TME, highlight key clinical milestones (e.g., FDA approval of a TIL product for melanoma in 2024), and outline bioengineering strategies-multi-antigen targeting, cytokine armoring, trafficking cues, and safety switches-that aim to overcome resistance and toxicity. We also review EV-based, cell-free strategies that retain tumor specificity with potentially improved safety and manufacturability. Finally, we discuss remaining barriers-standardized manufacturing, on-target/off-tumor effects, limited persistence-and propose rational combinations with checkpoint blockade, radiotherapy, and targeted agents. This overview positions immune cell-based therapy as a rapidly maturing, transformative approach for solid tumors.
    Keywords:  Cell therapy; Extracellular vesicles; Immune therapy; Solid tumor; TME
    DOI:  https://doi.org/10.1186/s12964-025-02632-y
  18. J Control Release. 2025 Dec 30. pii: S0168-3659(25)01197-6. [Epub ahead of print] 114583
      Logic-gated targeted therapies represent an emerging strategy to enhance specificity in cancer treatment by integrating multiple biological inputs to control therapeutic activation. Inspired by digital logic operations, these systems apply AND, OR and NOT functions to biomolecular processes to restrict activity to defined combinations of tumor-associated cues such as antigen co-expression, acidity or oxidative stress. This review develops a generalized logic-gating framework that unifies the terminology, design principles and mechanistic features of logic-gated systems across two major therapeutic modalities: CAR-T cells, which implement protein-based logic, and nanocarriers, which encode logic chemically. By formalizing concepts such as logic architecture, molecular implementation, mechanistic stage and input signal classification, this framework provides a cross-platform vocabulary for describing, comparing and designing logic-gated therapies. Applying this generalized model reveals characteristic differences in logic behavior across modalities. Protein-based CAR-antigen interactions often yield sharp, digital-like activation thresholds, whereas chemically responsive nanocarriers typically exhibit graded, analog-like release profiles. These behavioral patterns arise from fundamental differences in input signal types, molecular implementations and amplification mechanisms. Overall, this work positions molecular logic gating and multimarker targeting within a unified conceptual structure, clarifies current limitations and variability across platforms, and outlines opportunities for designing next-generation programmable cancer therapies with improved specificity and reduced on-target, off-tumor toxicity.
    Keywords:  CAR-T cell therapy; Logic-gated therapies; Multimarker targeting; Nanocarrier-based drug delivery; On-target off-tumor toxicity; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.jconrel.2025.114583
  19. Cancers (Basel). 2025 Dec 05. pii: 3892. [Epub ahead of print]17(24):
      Acute myeloid leukemia (AML) is a heterogeneous and aggressive hematologic malignancy with poor prognosis despite multiple available therapies. While chimeric antigen receptor (CAR) T-cell therapy has transformed the treatment of B-cell malignancies, its application in AML has been limited by early relapses and severe toxicities. Unlike B-cell antigens, most AML-associated surface antigens are also expressed on healthy hematopoietic stem and progenitor cells, creating significant risks of on-target/off-tumor toxicity and prolonged myeloablation. To address the scarcity of AML-specific targets, several innovative CAR strategies have been developed to enhance precision, safety, and efficacy. Logic-gated CARs improve selectivity through dual-antigen recognition or conditional activation. Drug-inducible and transient expression systems, as well as pharmacologic or suicide switches, enable controlled modulation or elimination of CAR cells to reduce toxicity. Adapter CAR platforms allow real-time, flexible targeting, while engineered modulation of gene expression or cytokine secretion enhances persistence and antitumor activity. Finally, alternative immune cells, including natural killer (NK) cells and macrophages, provide versatile platforms that may overcome limitations of conventional T-cell therapies, such as fratricide or challenges in allogeneic use. This review provides a comprehensive overview of these emerging CAR approaches, highlighting their advantages, limitations, and potential to expand immunotherapeutic strategies for AML.
    Keywords:  AML antigen landscape; CAR T cells; CAR-NK cells; CAR-γδ T cells; acute myeloid leukemia; allogeneic CAR products; armored CAR T cells; gene-edited immune cells; logic-gated CAR circuits; next-generation CAR therapies
    DOI:  https://doi.org/10.3390/cancers17243892
  20. Biomedicines. 2025 Nov 27. pii: 2903. [Epub ahead of print]13(12):
      Background/Objectives: Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is an established therapy for a range of hereditary disorders, including hemoglobinopathies, primary immunodeficiencies, and lysosomal storage diseases. Despite its long-standing use, rapid developments in donor availability, conditioning strategies, and supportive care have significantly broadened and refined its clinical application. This review combines recent evidence to clarify how these advances redefine current indications and therapeutic expectations. Methods: We critically analyze contemporary clinical data with a focus on elements that have undergone meaningful evolution-donor selection algorithms, conditioning intensity, graft manipulation, and post-transplant management. Comparative outcomes across major hereditary disease groups were examined to identify emerging trends in efficacy and safety. Results: The analysis highlights several novel shifts: expanding eligibility due to improved donor options, increasing reliance on reduced-toxicity regimens, and enhanced understanding of the mechanistic basis for hematologic, immunologic, and metabolic correction. These developments collectively improve survival and functional outcomes across diverse hereditary disorders. Conclusions: allo-HSCT remains a key therapeutic strategy for selected hereditary diseases, offering durable hematologic and metabolic correction. The prospective development of gene-addition and genome-editing therapies creates opportunities to complement-or in some cases replace-allo-HSCT, supporting the emergence of more personalized treatment approaches.
    Keywords:  allogeneic HSCT; hematopoietic stem cells; hemoglobinopathies; hereditary immunodeficiencies; lysosomal storage diseases (LSDs)
    DOI:  https://doi.org/10.3390/biomedicines13122903
  21. Int J Mol Sci. 2025 Dec 10. pii: 11918. [Epub ahead of print]26(24):
      Antibody-based therapeutics targeting tumor surface markers have transformed cancer treatment; however, their efficacy is frequently limited by tumor escape mechanisms such as antigen loss, phenotypic switching, and heterogeneous target expression. Beyond genetic or transcriptional changes, RNA alternative splicing (AS) has emerged as a central post-transcriptional mechanism driving antigenic diversity and immune escape. This review outlines how AS-generated isoforms remodel surface antigen structure and function across key therapeutic targets-including CD/19/CD20/CD22, EGFR/HER2, VEGF, and PD-1/PD-L1-thereby promoting resistance to monoclonal antibodies, antibody-drug conjugates, and immune checkpoint inhibitors. The aberrant activity of splicing regulators disrupts canonical exon selection, leading to altered receptor signaling or the secretion of soluble decoy isoforms that evade immune recognition. Emerging therapeutic strategies aim to counteract these processes through antisense oligonucleotide-mediated splicing correction, pharmacologic modulation of splicing regulators, and isoform-selective antibody or CAR-T designs. Collectively, understanding splicing-driven antigenic plasticity reveals an additional, dynamic layer of resistance regulation and provides a framework for developing RNA-informed precision antibody therapies designed to restore antigen expression, overcome immune escape, and enhance durable clinical responses.
    Keywords:  alternative splicing; antibody therapy resistance; immune checkpoint blockade; isoform diversity; precision oncology; splicing factors
    DOI:  https://doi.org/10.3390/ijms262411918
  22. BMJ Open. 2025 Dec 31. 15(12): e100304
       OBJECTIVES: Hospital data can inform decision-makers with real-time evidence, yet it remains underutilised. This study aims to compare international health technology assessment (HTA) and regulatory real-world evidence (RWE) guidance, focusing on their applicability to hospital data.
    STUDY DESIGN, SETTING AND PARTICIPANTS: We used a two-step sequential qualitative design: a scoping review and semi-structured interviews with HTA experts. We searched for RWE guidance for HTA in 12 countries: the UK, Germany, Italy, Spain, France, Finland, the Netherlands, Portugal, Denmark, Canada, the US and Australia, along with the European Medicines Agency and Food and Drug Administration. The expert interviews aimed to validate document selection and assess their applicability to hospital data. We analysed the interviews thematically.
    RESULTS: We identified 19 guidance documents providing recommendations for RWE. Of these, four documents explicitly provided recommendations tailored to hospital data, while two others did so implicitly. The scope, definition and applications of RWE vary among guidance. Recommendations across all agencies mainly address the clinical-effectiveness domain, with limited guidance on quality-of-life and patient-reported outcomes, and none on real-world cost. The interviews identified seven themes playing a role in using hospital data: data-related, generalisability, ethical/legal, organisational, communication, governance and technology-related. Barriers included data availability, access, timeliness, quality, validation and heterogeneity. HTA experts emphasised the need for standardised policies.
    CONCLUSIONS: There is a lack of harmonisation in assessing RWE among HTA and regulatory agencies. The available RWE guidance documents provide limited guidance on real-world hospital data. Considering their unique nature and to unlock their potential for HTA, we emphasise the need for more in-depth guidance tailored to the hospital context.
    Keywords:  Electronic Health Records; HEALTH ECONOMICS; Hospitals
    DOI:  https://doi.org/10.1136/bmjopen-2025-100304
  23. Transplant Cell Ther. 2025 Dec 29. pii: S2666-6367(25)02654-5. [Epub ahead of print]
      Graft-versus-host disease (GVHD) is still a significant challenge for allogeneic hematopoietic stem cell transplantation (allo-HSCT), resulting in substantial non-relapse mortality. Regulatory T cells (Tregs) are essential for modulating immune responses and maintaining tolerance, resulting in a promising therapeutic approach for GVHD management. The purpose of this study is to explore the immunomodulatory effect of Tregs in preventing and managing GVHD without sacrificing the graft-versus-leukemia (GVL) effect. Preclinical and clinical studies demonstrate that ex vivo-expanded Tregs, derived from donor peripheral blood or umbilical cord blood, effectively reduce GVHD incidence when infused prophylactically. Combination therapies, including Tregs with tacrolimus or invariant natural killer T (iNKT) cell activation via α-galactosylceramide, enhance Treg's efficacy and reduce required cell doses. Improved Treg stability and in vivo expansion can be achieved through advanced strategies such as rapamycin-assisted expansion and orthogonal IL-2/IL-2Rβ systems. These findings highlight Tregs' potential to mitigate GVHD without compromising GVL, offering a biologically favorable alternative to traditional immunosuppression. Further randomized trials are needed to standardize protocols and confirm long-term efficacy in the face of challenges in Treg isolation, expansion, optimal dosing, and infusion timing, which will lead to improved transplant outcomes.
    Keywords:  GVHD; GVL; Treg; allo-HSCT; immunomodulation
    DOI:  https://doi.org/10.1016/j.jtct.2025.12.991
  24. Clinicoecon Outcomes Res. 2025 ;17 975-989
       Introduction: Prescription drugs are excluded from Canada's federal legislation covering health care. Each provincial government has developed its own drug plan. To get new prescription medicines listed in these plans, developers must pass regulatory review, health technology assessment and price negotiation, and convince individual government plans to list their drugs. The objective of this research is to assess how many reimbursement recommendations issued by Canada's Drug Agency (CDA) have clinical and/or price conditions and what the consequences are.
    Methods: Data were obtained on drugs with CDA recommendations issued between January 2020 and December 2024, together with dates of price negotiations between the pan-Canadian Pharmaceutical Alliance (pCPA) and manufacturers by the end of July 2025 and listings in government plans relating to the same drugs by early November 2025.
    Results: Of 344 CDA recommendations, only three (0.9%) were unconditional reimbursement, 291 (84.6%) reimbursement with clinical criteria and/or a price condition, and 50 (14.5%) no reimbursement. Median time for CDA reviews was 221 days (interquartile range (IQR): 199-282 days). Where recommended to achieve cost-effectiveness of $50,000/quality-adjusted life-year, median reduction was 74.5% (IQR: 50.0%-90.0%). Median time for the pCPA to decide whether to negotiate was 128 days (IQR: 73-191 days) and median negotiation time was 131 days (IQR: 82-219 days). The median time between submission to CDA and pCPA outcome was 518 days (IQR: 394-633 days). Government drug plan listing rates for drugs successfully negotiated with the pCPA ranged from 58.6% to 91.6%. Five patients had prior-authorization requests to a private insurer for costly drugs denied because the drugs had conditional CDA recommendations.
    Conclusion: CDA and pCPA processes take considerable time and listing decisions by government drug plans add extra time before potential access by patients. Nearly all CDA reimbursement recommendations, which are intended for government drug plans (not private payers), are conditional.
    Keywords:  Canada; drug price negotiation; government drug plan coverage; health technology assessment; private insurance
    DOI:  https://doi.org/10.2147/CEOR.S567932
  25. J Immunother Cancer. 2025 Dec 31. pii: e013040. [Epub ahead of print]13(12):
       BACKGROUND: Chimeric antigen receptor (CAR)-T cell therapy has been successful for the treatment of hematological cancers but less effective against solid tumors, a phenomenon that results from the immunosuppressive nature of the tumor microenvironment. As a strategy to improve the treatment of solid tumors, we applied CAR therapy to dendritic cells (DCs) to generate CAR-DCs. The CAR targeted the human epidermal growth factor receptor 2 (HER2) which is overexpressed in breast cancer to defeat the immunosuppressive nature of the tumor microenvironment.
    METHODS: CAR-DCs were generated by lentiviral vector transduction of SAMHD1 knock-out murine bone marrow-derived DCs. The vectors coexpressed CD40L and a soluble form of programmed cell death 1 (PD-1), a checkpoint inhibitor. To increase the durability of CAR-DCs, a gene encoding the cytokine GM-CSF was introduced into the CAR vector. The CAR-DCs were injected into mice bearing B16.HER2 melanoma tumors. Tumor growth was measured, and T cell functionality was determined by IFNγ expression and in vitro cytolytic assay.
    RESULTS: CAR-DCs suppressed the growth of B16.HER2 tumors and induced the proliferation and activation of tumor-infiltrating cytolytic CD8+T cells. The PD-1 checkpoint inhibitor further augmented the antitumor response and prevented T cell exhaustion. Vectored expression of GM-CSF increased the durability of the antitumor response.
    CONCLUSIONS: CAR-DCs could be an effective strategy for therapies against solid tumors that should be further explored. The approach relies on the antigen-presenting ability of DCs and their role in T cell activation and can be coupled with checkpoint inhibition in place of monoclonal antibody treatment.
    Keywords:  Chimeric antigen receptor - CAR; Dendritic; Immune Checkpoint Inhibitor; Immunotherapy
    DOI:  https://doi.org/10.1136/jitc-2025-013040
  26. Front Immunol. 2025 ;16 1643176
      Autoimmune related interstitial lung disease can worsen between clinic visits, and episodic assessment may miss clinically important change. Digital health extends observation into daily life through home spirometry, wearable sensors, application based patient reported outcomes, and therapist supported telerehabilitation. This Review synthesizes recent evidence on feasibility and adherence, data quality and agreement with clinic assessments, patient experience and safety, and service integration for remote monitoring in autoimmune related interstitial lung disease. Device derived signals and patient generated health data show useful agreement with clinic measures when interpreted across repeated time points, and remote monitoring data can reveal actionable trends and support rehabilitation and self-management. Important limitations remain, including variability and artifacts, missing data, uneven interoperability, workload implications for services, and inequities in digital access. We outline a practical workflow for adoption that includes enrolment, training, quality checks, alert thresholds, and escalation to the multidisciplinary team, with attention to privacy, cost, and record integration. Remote monitoring can complement standard care by increasing observation frequency and patient support. Priorities for the field are to define clinically meaningful digital endpoints, evaluate effects on outcomes and use of resources, and develop strategies that sustain long term engagement.
    Keywords:  artificial intelligence - AI; autoimmune rheumatic diseases; interstitial lung disease (ILD); machine learning; remote monitor; wearables
    DOI:  https://doi.org/10.3389/fimmu.2025.1643176
  27. Sci Adv. 2026 Jan 02. 12(1): eaeb0821
      Epitopic peptides presented by class-I human leukocyte antigen (HLA-I) proteins provide the basis of immune surveillance by T cells. Conversely, reduced surface HLA-I expression is a hallmark of immune evasion by latent viral infections and cancer, which confounds the identification of peptide antigens and neoantigens. Here, we outline a system (HLA-Shuttle) for in vitro manipulation of cells with engineered components of the HLA-I processing machinery to confer a continuum of chaperoning activity throughout their trafficking pathway. HLA-Shuttle restores antigen presentation in immunologically cold neuroblastoma cells, enabling identification of multiple tumor-associated antigens with therapeutic potential. Cellular trafficking assays and single-particle tracking reveal a global stabilization of HLA-I molecules, extension of their cell-surface lifetime and microdomain formation. HLA-Shuttle can be used across a range of aberrant cellular states where low antigen expression remains a bottleneck for the identification of endogenous peptide antigens.
    DOI:  https://doi.org/10.1126/sciadv.aeb0821
  28. Signal Transduct Target Ther. 2025 Dec 30. 10(1): 428
      The mammalian target of rapamycin (mTOR) pathway is a central regulator of cellular growth, metabolism, and homeostasis, integrating a wide array of intracellular and extracellular cues, including nutrient availability, growth factors, and cellular stress, to coordinate anabolic and catabolic processes such as protein, lipid, and nucleotide synthesis; autophagy; and proteasomal degradation. The dysregulation of this signaling hub has broad implications for health and disease. To commemorate the 50th anniversary of the discovery of rapamycin, we provide a comprehensive synthesis of five decades of mTOR research. This review traces the historical trajectory from the early characterization of the biological effects of rapamycin to the elucidation of its molecular target and downstream pathways. We integrate fundamental and emerging insights into the roles of mTOR across nearly all domains of cell biology and development, with a particular focus on the expanding landscape of therapeutic interventions targeting this pathway. Special emphasis is placed on the crosstalk between mTOR signaling and mitochondrial regulation, highlighting the mechanisms by which these two metabolic hubs co-regulate cellular adaptation, survival, and disease progression. The dynamic interplay between mTOR and mitochondrial networks governs key aspects of bioenergetics, redox balance, and cell fate decisions and is increasingly implicated in pathophysiological contexts ranging from cancer and aging to neurodegenerative and immune disorders.
    DOI:  https://doi.org/10.1038/s41392-025-02493-4
  29. Curr Opin Organ Transplant. 2026 Feb 01. 31(1): 21-26
       PURPOSE OF REVIEW: Across the world, several solid organ xenotransplants have been reported as being provided to deceased people and to living patients. In the United States, xenotransplants to living patients have been authorized under the Food and Drug Administration's Expanded Access program, and clinical liver and kidney xenotransplants have also been reported in China. During 2025, the first clinical trials of kidney and liver xenotransplants have been approved in the United States. These developments make it necessary to understand the regulatory and governance issues and challenges raised by clinical xenotransplants.
    RECENT FINDINGS: Key regulatory and governance issues remain to be addressed before xenotransplant clinical trials begin, including identifying the responsible regulator, drafting informed consent protocols, and establishing long-term monitoring regimens. International cooperation and collaboration are key to establishing appropriate and effective regulatory regimes and frameworks which enable science to proceed while offering the necessary protections to those involved. Public awareness, education and trust are central to the success of clinical xenotransplantation.
    SUMMARY: Starting xenotransplant clinical trials too soon and without appropriate regulation and governance, may affect public trust in this biotechnology specifically and science more generally. The possible risks of xenotransplantation necessitate exploration of global harmonization and regulatory frameworks for clinical xenotransplantation.
    Keywords:  clinical xenotransplantation; governance; law; public trust; regulation
    DOI:  https://doi.org/10.1097/MOT.0000000000001257
  30. Adv Exp Med Biol. 2026 ;1490 291-298
      Huntington's Disease (HD) is an inherited, progressive, deteriorating, and non-curable disease affecting physical and cognitive states. Recent advancements in cell and gene therapy have brought in new treatment options that challenge Huntington's Disease, with the ultimate goal to modify its trajectory. This article emphasizes the role of nurses in Huntington's Disease advanced treatments. Furthermore, it underlines the importance of patient-oriented care as well as the ethical considerations that may occur.
    Keywords:  Cell and gene therapy; Huntington’s disease; Nursing care
    DOI:  https://doi.org/10.1007/978-3-032-03402-1_31
  31. Ther Adv Neurol Disord. 2025 ;18 17562864251401510
      Therapeutic plasma exchange (PLEX) is a powerful and fast-acting immunomodulating therapy that is underutilized for autoimmune neurological disorders. Here, we present the largest collection of real-world experiences with PLEX procedures to date in the treatment of autoimmune neurological conditions, supporting its safety and clinical benefits with patient cases and corresponding patient videos. Our collective real-world experience with PLEX spans over 67 years, 90,210 procedures, and includes nine double-blind randomized controlled and unblinded studies serving as principal investigators. Case histories and videos of our patients demonstrate when and how PLEX should be used, identify barriers to using PLEX, and ways to overcome these barriers. Specific protocol details are shared of how to treat an acute or chronic phase of a disease. If used appropriately and early in the disease course for both acute and chronic progressive phases, PLEX can safely change the trajectory of many autoimmune neurological disorders in both outpatient and inpatient settings.
    Keywords:  PLEX; arterial puncture; chronic inflammatory demyelinating polyneuropathy; healthcare insurance; multiple sclerosis; myasthenia gravis; neuromyelitis optica spectrum disorders; plasma exchange; plasmapheresis; polymyositis; venous access
    DOI:  https://doi.org/10.1177/17562864251401510