bims-flamet Biomed News
on Cytokines and immunometabolism in metastasis
Issue of 2026–03–01
twenty-two papers selected by
Peio Azcoaga, Biodonostia HRI



  1. Curr Issues Mol Biol. 2026 Jan 30. pii: 155. [Epub ahead of print]48(2):
      The tumor microenvironment (TME) is a highly dynamic and heterogeneous ecosystem composed of cancer cells, stromal components, immune cells, and extracellular matrix [...].
    DOI:  https://doi.org/10.3390/cimb48020155
  2. Discov Oncol. 2026 Feb 25.
      
    Keywords:  Angiogenesis; Lipid metabolic reprogramming; Tumor metabolism; Tumor microenvironment (TME)
    DOI:  https://doi.org/10.1007/s12672-026-04645-6
  3. Cancer Discov. 2026 Feb 19. OF1
      Two recent studies of CAR T cells targeting tumor-associated macrophages have shown that "armoring" these engineered cells with the ability to express the cytokine IL12 makes them more effective at eradicating solid tumors and leads to sustained remodeling of the immunosuppressive tumor microenvironment.
    DOI:  https://doi.org/10.1158/2159-8290.CD-NW2026-0016
  4. RSC Adv. 2026 Feb 16. 16(11): 10261-10283
      Ferroptosis, a distinct form of programmed cell death driven by iron-dependent lipid peroxidation, has emerged as a critical player in cancer biology, influencing both tumor progression and therapeutic responses. This review explores the multifaceted role of ferroptosis within the tumor microenvironment (TME), focusing on its dual potential to promote anti-tumor immunity and immune evasion. Key molecular mechanisms regulating ferroptosis, including the roles of GPX4, SLC7A11, and ACSL4, are examined alongside their interplay with immune cells such as CD8+ T cells, dendritic cells, and macrophages. The review addresses the immunosuppressive effects of ferroptosis-induced signals such as prostaglandin E2 and damage-associated molecular patterns that foster tumor growth. Furthermore, therapeutic strategies leveraging ferroptosis to overcome resistance in cancer treatment, including its integration with immunotherapy and radiotherapy, are discussed. This study underscores the potential of targeting ferroptosis to enhance cancer therapy while emphasizing the need for further research to optimize its application in immunotherapy.
    DOI:  https://doi.org/10.1039/d5ra08026f
  5. Biomedicines. 2026 Jan 28. pii: 294. [Epub ahead of print]14(2):
      This review describes the immunosuppressive effect of secreted phosphoprotein 1 (SPP1)+ tumor-associated macrophages (TAMs) in coordinating the tumor microenvironment (TME) as a functionally unique myeloid cell subgroup. SPP1+ TAMs transcend the traditional M1/M2 paradigm and represent a group of cells that are widely found in various cancer types. SPP1+ TAMs have the characteristics of high expression of SPP1 and promoting immune escape, matrix remodeling and metastasis. We clarify the dual developmental source of SPP1+ TAMs, and introduce the activation process of SPP1+ TAMs through recruitment, polarization and epigenetic locking. After SPP1+ TAMs are activated, they are strategically enriched in the tumor core and tumor marginal area to play their functions. Functionally, SPP1+ TAMs mainly promote the progression of tumors through three mechanisms: (1) Interacting with cancer-associated fibroblasts (CAFs): constructing an immunoexcluded fibrotic niche; (2) Multiple regulation of immune cells; (3) Promoting tumor metastasis and the construction of pre-metastatic niche (PMN). Overall, this review aims to provide a comprehensive overview of the mechanisms mediated by SPP1+ TAMs in the TME, and emphasize their unique role in cancer progression. At the same time, the treatment strategies targeting them are further explored, highlighting their potential as precise therapeutic targets for tumor treatment.
    Keywords:  SPP1; TAMs; TME; cancer; fibrosis; immunosuppression
    DOI:  https://doi.org/10.3390/biomedicines14020294
  6. FEBS Lett. 2026 Feb 24.
      Liver cancer stands as the sixth leading cause of cancer-related deaths globally, with hepatocellular carcinoma (HCC) being the most frequently diagnosed subtype. The hepatic tumor microenvironment (TME) comprises a complex array of cellular and non-cellular components, including activated hepatic stellate cells (HSCs), tumor-associated macrophages (TAM), endothelial cells, immune cells, and non-cellular elements such as growth factors, proteolytic enzymes, inhibitors, and extracellular matrix (ECM) proteins. The initiation and progression of HCC involve intricate interactions among hepatocytes, tumor cells, and non-tumor cells, including liver-resident non-parenchymal cells (NPCs). The Hippo-YAP pathway plays a crucial role in tumor development and initiation. YAP/TAZ, as primary effectors of the Hippo pathway, intricately connect with other signaling pathways relevant to tumors. YAP promotes the growth of cancer stem cells, the development of malignant phenotypes, and drug resistance, contributing significantly to cancer growth. This review focuses on the role of YAP in stromal cells as a mediator of HCC. We aim to present a comprehensive overview, not only consolidating existing knowledge but also paving the way for innovative exploration in pursuing effective therapeutic strategies against HCC.
    Keywords:  Hepatocellular carcinoma; Stromal cells; Therapeutic targeting; Tumor microenvironment; YAP
    DOI:  https://doi.org/10.1002/1873-3468.70310
  7. J Immunother Cancer. 2026 Feb 24. pii: e014457. [Epub ahead of print]14(2):
      Tumor-associated macrophages are key myeloid cells in the tumor microenvironment (TME), acting as essential orchestrators of innate and adaptive immune responses. The efficacy of current antitumoral treatments can be promoted by macrophages, thanks to their phagocytosis, tumoricidal activity, and eliciting of adaptive immunity; or restricted by their expression of inhibitory counter-receptors (such as programmed death-ligand 1 or signal regulatory protein alpha). Furthermore, the continuous recruitment of these myelomonocytic cells into tumor tissues makes them attractive candidates for cell therapy with the development of chimeric antigen receptor (CAR) effector cells. This evidence highlights the strong therapeutic potential of macrophage engineering for the treatment of solid tumors. In this line of research, Du et al developed pArg1-CD47 CAR-Mφ based on intrinsic Arg1 promoter responsiveness for TME-specific activation of cytotoxicity, effectively overcoming SIRPα inhibition against CD47+cancer cells. In preclinical murine models of breast and gastric cancer, this macrophage cell therapy demonstrated significant regression of established tumors with minimal toxicity towards erythrocytes. Although translating this work from mice to humans remains a significant challenge, it provides hope for the design of myeloid cell therapies with antitumoral efficacy and safe profile for solid tumors.
    Keywords:  Chimeric antigen receptor - CAR; Immunotherapy; Myeloid; Solid tumor; Tumor microenvironment - TME
    DOI:  https://doi.org/10.1136/jitc-2025-014457
  8. Cancer Lett. 2026 Feb 20. pii: S0304-3835(26)00111-4. [Epub ahead of print]645 218348
      Immune checkpoint inhibitors show insufficient efficacy against pancreatic ductal adenocarcinoma (PDAC). The tumor microenvironment (TME) has a remarkable influence on responsiveness to cancer immunotherapy. The aim of this study was to investigate immunosuppressive characteristics of TME in PDAC tissues. The flow cytometry (FCM) of PDAC surgical specimens revealed that the profile of tumor-infiltrating leukocytes was classified into myeloid cell- and T-cell-dominant subtypes; the myeloid subtype was associated with poorer patient outcomes. Myeloid-derived suppressor cells (MDSCs) showed the highest hazard ratio among various myeloid cell types. Single-cell RNA sequencing and FCM revealed that most MDSCs, but not lymphocytes, in PDAC tissues characteristically express CD74. Macrophage migration inhibitory factor (MIF), a CD74 ligand, was highly expressed in cancer-associated fibroblasts (CAFs) and cancer cells. Spatial transcriptomics demonstrated that the MIF-CD74+ myeloid cell interaction was recognized in CAF-dominant areas in PDAC tissue. CAFs expressing immune suppressor molecules such as MFAP5 and LRRC15 were consistent with MIF+ CAFs. Furthermore, MIF+ CAFs enhanced the migratory activity of MDSCs and promoted MDSC induction and activation. In the murine model, MDSCs were significantly increased in MIF-expressing PDAC tumors, as were CD74+ M-MDSCs per M-MDSC, confirming in vivo interaction between CD74 and MIF. MDSCs play a crucial role in creating an immunosuppressive TME in PDAC; the MIF-CD74 axis drives interactions between MDSCs and CAFs.
    Keywords:  CD74; Cancer-associated fibroblasts; Macrophage migration inhibitory factor; Myeloid-derived suppressor cells; Pancreatic ductal adenocarcinoma
    DOI:  https://doi.org/10.1016/j.canlet.2026.218348
  9. Metabolites. 2026 Feb 20. pii: 145. [Epub ahead of print]16(2):
      The tumor microenvironment (TME) plays a key role in driving tumor progression, metastasis, and resistance to therapy. The TME is a highly variable ecosystem composed of both cancer and surrounding normal cells, immune survey cells and the extracellular matrix, also composed of signaling molecules that mediate interactions between them. Blood cancer cells pose a unique challenge because of their circulation and widespread distribution along with their capacity to invade various niches, interacting with a wide range of host cells such as fibroblasts, immune cells, endothelial cells, and adipocytes. Metabolism reprogramming in this tumor context, notably referring to elevated cholesterol and fatty acid metabolism, emerges as a crucial event in shaping an immune-suppressive microenvironment that promotes tumor progression. Cholesterol and fatty acids are supplied by both de novo biosynthesis and exogenous uptake from lipoproteins. Lipoproteins are pseudo-micellar structures, designed to transport essential water-insoluble metabolites, including triacylglycerols and cholesterol, in the plasma, lymph, and interstitial fluids. A number of studies have reported abnormal circulating lipoprotein levels in leukemic patients and have suggested that lipoproteins are key for cancer cells to thrive. However, the role of lipoprotein metabolism in cancer cells in the context of the TME is still incompletely discussed so far. The aim of this review is to consider the importance of lipoprotein metabolism in shaping the tumor microenvironment in the context of hematological malignancies.
    Keywords:  leukemia; lipoprotein metabolism; lymphoma; tumor progression
    DOI:  https://doi.org/10.3390/metabo16020145
  10. Curr Issues Mol Biol. 2026 Feb 12. pii: 202. [Epub ahead of print]48(2):
      Immune response evasion is one of the hallmark features of cancer, which is not only the basis for cancer progression and metastasis but also affects the clinical management of cancer. Tumor immune evasion is mainly attributed to the dynamic and immunosuppressive tumor microenvironment (TME), which is regulated by a complex system including immunosuppressive cells and cytokines. Interleukin-18 (IL-18) is an important cytokine that plays a multifaceted role in immune system regulation, and its function is strictly regulated by the natural antagonist IL-18 binding protein (IL-18BP). IL-18 exhibits context-dependent immunoregulatory characteristics (acting as a "context resistor") during tumor occurrence and progression, which is closely related to cancer type, stage, and the signaling network of the tumor microenvironment. The multifaceted functions of IL-18 have been utilized in cancer treatment to reduce the phenomenon of immune escape of tumors. With the latest advancements in cancer research related to IL-18, it is necessary to integrate the latest research findings to deepen the understanding of the mechanism of tumor immune escape and promote the improvement of cancer treatment levels. This review will systematically elaborate on the action mode, core regulatory mechanism and key signaling pathways of IL-18 in tumor immune evasion, analyze the heterogeneity patterns associated with its context-dependent effects, comprehensively sort out the core obstacles in clinical translation, and at the same time, envision new precision treatment strategies based on IL-18 regulation.
    Keywords:  IL-18; IL-18BP; immune evasion; tumor immunity; tumor microenvironment
    DOI:  https://doi.org/10.3390/cimb48020202
  11. Front Immunol. 2026 ;17 1756299
      Brain metastasis significantly worsens prognosis in late-stage cancer., with Its treatment hindered by the blood-brain barrier (BBB) and an immunosuppressive tumor microenvironment. Within this environment, tumor-associated macrophages (TAMs) represent the predominant immune population. Through their roles in immune modulation, angiogenesis, and tumor invasion, TAMs are critical drivers of disease progression. TAMs are highly heterogeneous. While traditionally categorized into M1 (anti-tumor) or M2 (pro-tumor) phenotypes, this dichotomy is an oversimplification. Recent single-cell studies have revealed a spectrum of functional subpopulations, such as lipid-associated, interferon-responsive, and pro-angiogenic TAMs, with M2-like states typically prevailing to mediate immunosuppression. This review explores the diversity and functions of TAMs in brain metastasis. We first detail their biological characteristics, including origins, heterogeneous subtype classifications (e.g., lipid-associated macrophages that extend beyond the simple M1/M2 dichotomy), and polarization states. We further discuss how polarization is regulated by signaling pathways (e.g., STAT, NF-κB) and microenvironmental factors (e.g., hypoxia, metabolic reprogramming). We examine TAM roles from pre-metastatic niche formation to tumor colonization, using breast and lung cancer brain metastases to illustrate how TAMs disrupt the BBB and facilitate immune evasion through molecules like ANGPTL4 (angiopoietin-like 4) and MMP9. Key pathways of TAM-tumor cell interactions, including neuro-cancer interactions, immune-metabolic regulation, and exosome-mediated communication, are also discussed. Targeting TAMs offers promising therapeutic avenues. These strategies include reprogramming TAMs (e.g., using CSF1R inhibitors), combining TAM-targeted therapy with immune checkpoint inhibitors, and developing novel approaches such as nanotechnology and CAR-macrophages. However, several challenges remain, including TAM heterogeneity, lack of targeting specificity, and the obstacle of BBB delivery. Future research should leverage technologies like single-cell sequencing and spatial transcriptomics to decode TAM heterogeneity, and develop personalized treatments based on biomarkers such as GPNMB and TRAIL, aiming to improve patient outcomes in brain metastasis.
    Keywords:  brain metastasis; immunosuppression; immunotherapy; tumor microenvironment; tumor-associated macrophages
    DOI:  https://doi.org/10.3389/fimmu.2026.1756299
  12. Front Oncol. 2025 ;15 1583295
      Exosomes are important intercellular communication substances that connect the intercellular communication between the tumor microenvironment and the premetastatic microenvironment during tumor progression. By carrying different regulatory substances, such as proteins, cytokines, nucleic acids, etc., to regulate tumor progression, including angiogenesis, invasion, metastasis, drug resistance and other aspects. In addition to their potential as diagnostic markers, exosomes can also be used as excellent drug delivery carriers. Due to their excellent targeting and histocompatibility, exosomes have considerable application prospects in tumor therapy. This reviews recent studies on tumor-related exosomes, summarizes the mechanisms of intercellular communication and regulation of exosomes in tumor microenvironment and pre-metastasis microenvironment, and summarizes the current research progress on exosomes in tumor therapy.
    Keywords:  exosome; pre-metastatic microenvironment; progression; treatment; tumor microenvironment
    DOI:  https://doi.org/10.3389/fonc.2025.1583295
  13. Int J Cancer. 2026 Feb 25.
      Discoidin domain receptors (DDRs) are nonintegrin collagen receptors which could be activated by various collagens. Overexpressed in numerous cancers, DDRs participate in tumorigenesis, tumor growth, dissemination, and metastasis. Immune checkpoint inhibitors (ICIs) have demonstrated low response rates in tumors such as head and neck cancer and pancreatic cancer, possibly due to the insufficient presence of effector T cells and the abundant collagen fibers in the tumor microenvironment. Recently, several studies indicate that DDRs account for ICIs resistance. For instance, DDR1 can prevent the anti-tumor immune responses via mediating the rearrangement of collagen fibers, increasing the secretion of interleukin-18 (IL-18) as well as facilitating the formation of neutrophil extracellular traps (NETs). DDR2 may participate in the establishment of immunosuppressive tumor microenvironment by recruiting myeloid-derived suppressor cells (MDSCs) and promoting the M2 polarization of macrophages. Notably, the interaction between collagens and immune cells also acts as a pivotal role in mediating tumor immune escape. Targeting DDRs and upstream regulators including collagen has been reported to significantly restore the antitumor immunity or inhibit tumor development, such as utilizing DDR1 inhibitors via AI screening from FDA-approved therapeutics or natural products, and strategies for collagen synthesis inhibition or collagen degradation. However, the above approaches are largely limited to preclinical studies and still warrant further validation in clinical trials. Based on the current evidences, DDRs serve as promising targets for improving the efficacy of ICIs against cancers; more studies are anticipated to reveal unclarified mechanisms of DDRs in regulating anti-tumor immunity.
    Keywords:  collagen fiber rearrangement; discoidin domain receptors; immunotherapy; tumor immunity
    DOI:  https://doi.org/10.1002/ijc.70398
  14. Blood Sci. 2026 Mar;8(1): e00270
      Hematological malignancies, including leukemia, lymphoma, and multiple myeloma, develop within and remain dependent on a complex and dynamic tumor microenvironment (TME). Malignant cells interact continuously with the cellular and molecular components of the TME, which play a critical role in shaping disease progression, therapeutic response, and immune evasion. The TME comprises mesenchymal stromal cells, immune cells, fibroblasts, endothelial cells, and a range of signaling molecules such as chemokines, cytokines, and extracellular vesicles, embedded within a heterogeneous extracellular matrix (ECM). This integrated network, along with recently established mechanisms, establishes a supportive niche that promotes malignant cell survival, clonal evolution, immune modulation, and therapy resistance. This review examines the cellular and molecular architecture of the hematologic TME and its influence on chemoresistance and immune suppression. It further discusses therapeutic interventions that aim to disrupt or reprogram the TME, thereby restoring therapeutic sensitivity and enhancing immune-mediated clearance.
    Keywords:  Chemotherapy resistance; Hematological malignancy; Immune evasion; Leukemia; Lymphoma; Multiple myeloma; Tumor microenvironment
    DOI:  https://doi.org/10.1097/BS9.0000000000000270
  15. J Leukoc Biol. 2026 Feb 26. pii: qiag026. [Epub ahead of print]
      Tumor-associated macrophages (TAMs) are a critical component of the immune response to cancer, and their role in modulating cancer progression is well-recognized. Macrophages express pattern-recognition receptors, including Class A Scavenger Receptors (SR-A), which are pivotal in regulating macrophage activation and polarization into distinct phenotypes. SR-A expression is generally correlated with altered cytokine expression indicative of a tumor-supportive M2 macrophage phenotype. While evidence links an increased prevalence of SR-A-expressing TAMs to worse patient outcomes in breast cancer, a definitive role for SR-A and its potential ligands in cancer remains to be fully established. We previously reported that the fibroblast-activated proteinase (FAP)-cleaved collagen is a ligand for SR-A. This study was conducted to assess the role of FAP and SR-A expression in breast cancer. Using mouse models of spontaneous breast cancer, we found that the absence of SR-A, but not FAP, expression significantly delayed the development of palpable tumors and decreased the number of lung metastases in tumor-bearing mice. A soluble SR-A protein was used to demonstrate that SR-A binds to glycans on the surface of breast cancer cells. We used single-cell RNA sequencing and flow cytometry of isolated TAMs and identified a distinct SR-A-dependent TAM subpopulation characterized by high arginase 1 (Arg1) gene expression. Pathway analysis of TAMs associates SR-A expression with activation of transcriptional programs linked to immune-suppressive macrophage phenotypes. These results define a contributory role for SR-A in breast cancer progression and provide new insights into the complex interactions between TAMs and cancer cells in the tumor microenvironment.
    Keywords:  Breast Cancer; SR-A; Tumor microenvironment; Tumor-associated macrophages
    DOI:  https://doi.org/10.1093/jleuko/qiag026
  16. Biomolecules. 2026 Feb 04. pii: 246. [Epub ahead of print]16(2):
      Ovarian cancer (OC) is a particularly lethal gynecological malignancy with few treatment options due to its late-stage diagnosis, extensive genetic heterogeneity, and frequent development of resistance to existing therapies. Immunotherapy has revolutionized the management and clinical outcome of numerous solid tumors, but its clinical benefit for OC has been limited, in part due to an extremely immunosuppressive tumor microenvironment (TME) and diverse, overlapping immune evasion mechanisms. In this review, we present a comprehensive and timely synthesis of next-generation immunotherapeutic approaches for ovarian cancer, emphasizing strategies that overcome the immunosuppressive tumor microenvironment and improve clinical responsiveness. We describe the emerging molecular mechanisms of immune evasion in OC, including altered antigen presentation, inhibition of T-cell activation (e.g., via immunological checkpoints, metabolic reprogramming), polarization of tumor-associated macrophages (TAMs), and dysfunction of natural killer (NK) cells. We also critically examine several emerging therapeutic approaches, including combination immune checkpoint blockade (ICB), bispecific T-cell engagers (BiTEs), neoantigen-based vaccines, chimeric antigen receptor (CAR)-T- and CAR-NK-cell therapies, oncolytic viruses (OVs), and nanoparticle-mediated immunomodulation. In addition, we highlight recent advances in tumor microenvironment-targeted therapies for ovarian cancer, focusing on strategies that modulate non-lymphoid components such as cancer-associated fibroblasts (CAFs), hypoxia-driven signaling, and the PI3K/AKT/mTOR axis to enhance antitumor immune responsiveness. Finally, we discuss how predictive biomarkers, multi-omics systems, and patient-derived organoid models are accelerating the development and deployment of precision immunotherapies for OC. We would like to highlight the translational promise of next-generation immunotherapies and identify novel molecular targets that may be leveraged to achieve durable responses in OC.
    Keywords:  immune evasion; immunosuppressive; immunotherapy; next-generation therapeutics; ovarian cancer; tumor microenvironment
    DOI:  https://doi.org/10.3390/biom16020246
  17. Biomol Biomed. 2026 Feb 27.
      Breast cancer progression is influenced not only by intrinsic tumor alterations but also by reciprocal interactions with the tumor microenvironment (TME), a complex ecosystem comprising fibroblasts, immune and endothelial cells, adipocytes, extracellular matrix components, soluble mediators, and extracellular vesicles. This review synthesizes recent basic and translational research on how TME-derived signals activate dysregulated signaling pathways, including the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR), transforming growth factor beta/SMAD (TGF-β/SMAD), Janus kinase/signal transducer and activator of transcription (JAK/STAT), mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), Wingless-related integration site/beta-catenin (Wnt/β-catenin), Notch, Yes-associated protein/transcriptional co-activator with PDZ-binding motif (YAP/TAZ), and nuclear factor kappa B (NF-κB). These pathways promote key processes such as invasion, angiogenesis, adaptation to hypoxia, epithelial-mesenchymal transition, immune evasion, cancer stemness, and therapy resistance. We emphasize convergent findings that indicate the feedback loop between tumor cells and the TME sustains plasticity and drug-tolerant states. Additionally, we summarize emerging therapeutic strategies, including stromal and extracellular matrix normalization, immunotherapy combinations, pathway-targeted inhibitors, and nanotechnology-enabled drug delivery. A comprehensive understanding of TME-signaling crosstalk is crucial for overcoming therapeutic resistance in breast cancer.
    DOI:  https://doi.org/10.17305/bb.2026.13708
  18. Front Immunol. 2026 ;17 1755073
      Glioblastoma (GBM) is the most common and aggressive brain tumor in adults, and current treatments remain poorly efficient. In this context, immunotherapies may represent promising strategies. However, their efficacy is often limited by a strong negative impact of the tumor microenvironment (TME) of glioblastoma. Several factors such as tumor cells mutational profile, previous lines of conventional treatments, or biological factors, have been shown as involved in TME modulation. In this review, our goal is to give an overview of the main modulating factors of the TME of glioblastoma tumors. We will also highlight the importance of developing complex and integrative models to study this microenvironment. At the end, by highlighting critical components of the glioblastoma microenvironment, this review aims to support the development of next-generation, more effective and personalized immunotherapeutic strategies.
    Keywords:  glioblastoma; immunotherapy; microenvironment; modulating factors; myeloid cells
    DOI:  https://doi.org/10.3389/fimmu.2026.1755073
  19. Front Immunol. 2026 ;17 1744671
      Dendritic cells (DCs) are central orchestrators of antitumor immunity, but their functions are markedly curtailed by glycolysis-dominated metabolic constraints in the tumor microenvironment (TME). This review focuses on two interconnected dimensions: tumor-derived metabolic stressors that suppress DC activation and the intrinsic metabolic programs of DC subsets that define their immunogenic potential. Lactate accumulation, hypoxia, adenosine signaling, and lipid overload disrupt antigen cross-presentation, type I interferon (IFN-I) production, and DC migration, collectively biasing DCs toward tolerogenic or checkpoint-high states. At the same time, subset-specific metabolic wiring-such as reliance on oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) in conventional type 1 DCs (cDC1s), glycolysis-dependent Th17-skewing capacity in conventional type 2 DCs (cDC2s), and pronounced hypoxia sensitivity in plasmacytoid DCs-creates distinct vulnerabilities that can be therapeutically exploited. We further summarize emerging strategies to restore DC metabolic fitness, including blockade of tumor glycolysis, intrinsic DC metabolic rewiring, modulation of immunometabolites and redox balance, use of natural products and nanomaterials, and rational combinations with radiotherapy or immune checkpoint blockade. Finally, we outline translational priorities such as single-cell and spatial mapping of DC metabolic heterogeneity, development of metabolism-linked biomarkers, and integration of DC-targeted interventions into existing immunotherapy frameworks. Together, these insights position DC metabolism as a critical lever to reprogram the TME and to enable more durable antitumor immunity.
    Keywords:  dendritic cells; glycolysis; immune tolerance; immunotherapy; metabolic reprogramming; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2026.1744671
  20. Biochem Biophys Res Commun. 2026 Feb 25. pii: S0006-291X(26)00291-3. [Epub ahead of print]810 153527
      The tumor microenvironment (TME) exerts a pivotal influence on malignant phenotypes, including invasion, metastasis, immune evasion, and therapeutic resistance, thereby dictating clinical outcomes and patient prognosis. Consequently, a comprehensive elucidation of TME dynamics is of paramount importance. To address this, the development of in vitro tumor models capable of faithfully recapitulating its inherent complexity is indispensable. In this study, we engineered millimeter-scale, high-density 3D tumor constructs that recapitulate the intricate architectural and functional hallmarks of the in vivo TME. Within this biomimetic platform, reciprocal crosstalk with cancer cells induced the differentiation of cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). Furthermore, we successfully modeled divergent immunophenotypes, characterized as "hot" and "cold" tumors, and integrated a hierarchical vascular network comprising venous and capillary-like structures. Collectively, this construct accurately mirrors the in vivo TME, providing a robust platform for modeling complex tumor ecosystems and offering substantial potential to catalyze advancements in cancer research and drug discovery.
    Keywords:  High cell density; Hot/cold tumor; Millimeter scale; Tumor construct; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.bbrc.2026.153527
  21. Front Immunol. 2026 ;17 1724756
      OX40 (CD134/TNFRSF4), a costimulatory receptor of the TNF receptor superfamily ((TNFRSF), has emerged as a compelling immuno-oncology target given its capacity to amplify T-cell activation, sustain effector and memory responses, and remodel the tumor microenvironment (TME). This review provides a comprehensive synthesis of OX40 biology from molecular architecture to pathway-specific signaling programs, emphasizing its distinct yet interconnected roles across CD4+ T-cell subsets, CD8+ T cells, T follicular helper cells, and regulatory T cells (Tregs). We further summarize the landscape of OX40 expression across major solid tumors, highlighting its heterogeneous prognostic significance and the immune-contextual factors that determine therapeutic responsiveness. Although early-phase clinical studies of OX40 agonists have demonstrated favorable tolerability and robust pharmacodynamic activation, their antitumor efficacy either as monotherapy or in combination with PD-1/PD-L1 or CTLA-4 inhibitors has remained modest. Mechanistic barriers such as transient OX40 expression kinetics, Treg counteractivation, metabolic suppression, and insufficient FcγR-mediated crosslinking likely underlie this translational gap. Emerging bispecific antibody platforms and OX40-integrated combinatorial regimens offer renewed opportunities to overcome these limitations by enabling spatially controlled receptor clustering, TME-selective activation, and multi-pathway synergy. Future translational success will require refined dosing strategies, optimized antibody engineering, biomarker-guided patient selection, and integrated approaches that align OX40 activation with favorable immune dynamics in the TME.
    Keywords:  OX40; cancer immunotherapy; combination therapy; costimulatory signaling; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2026.1724756
  22. Front Immunol. 2026 ;17 1743920
      The interplay between the immune system and leukemia presents major challenges to effective therapy development. This Review examines mechanisms of immune evasion across leukemia subtypes, emphasizing T-cell exhaustion, regulatory T cells (Tregs), and antigen-presentation deficits. Globally, leukemia remains a significant burden, with approximately 460,000 new cases and 320,000 deaths estimated in 2021 alone. Recent studies reveal how the tumor microenvironment (TME) shapes immune behavior and how leukemic cells remodel it to support survival and therapeutic resistance. We illustrate these adaptive processes, highlighting the contributions of the bone-marrow niche and B-cell dysregulation in chronic lymphocytic leukemia (CLL). We further discuss implications for immunotherapy, noting that agents like magrolimab (anti-CD47) combined with azacitidine have demonstrated objective response rates (ORR) exceeding 80% in early-phase AML trials, though challenges such as on-target anemia persist. By integrating current evidence from preclinical metabolic profiling to Phase 3 clinical data on E-selectin inhibition (uproleselan)-we clarify the immune landscape of leukemia and outline avenues for innovative treatments. Ultimately, this Review underscores the need for multifaceted immunotherapeutic approaches that account for the complex interactions within the TME.
    Keywords:  T-cell exhaustion; bone marrow niche; immune evasion; immunotherapy; leukemia; therapeutic resistance; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2026.1743920