bims-tuinly Biomed News
on Tumor-infiltrating lymphocytes therapy
Issue of 2026–03–15
twenty papers selected by
Pierpaolo Ginefra, Ludwig Institute for Cancer Research



  1. Asian Pac J Cancer Prev. 2026 Mar 01. pii: 92106. [Epub ahead of print]27(3): 1123-1133
       OBJECTIVES: This study aims to investigate the clinicopathological significance and prognostic impact of SLFN11 expression and tumor-infiltrating lymphocytes (TILs) in high-grade and low-grade ovarian serous carcinoma.
    METHODS: A total of 70 patients diagnosed with high-grade and low-grade serous carcinoma were retrospectively analyzed. Clinical data, including age, Karnofsky Performance Status (KPS), CA125 levels, treatment details, and survival outcomes, were collected. Immunohistochemistry was used to assess SLFN11 expression in tumor cells and TILs. Statistical correlations were performed with chemotherapy response, recurrence, progression-free survival (PFS), and overall survival (OS).
    RESULTS: High SLFN11 expression was significantly associated with better response to neoadjuvant chemotherapy (p = 0.003), higher histopathologic chemotherapy response score (p = 0.026), lower recurrence rate (p = 0.037), and improved survival outcomes (p < 0.001). High SLFN11 expression had significantly longer PFS (median= 33.05 months) and OS (median= 66.91 months), compared to those with low SLFN11 expression (median PFS =7.60 and median OS = 31.50, p<0.001). Similarly, high TILs count was associated with improved response to neoadjuvant chemotherapy (p = 0.008) and higher response score (p = 0.007). TILs-high patients had longer median PFS (25.52 months) and median OS (68.24 months) than TILs-low patients (median PFS = 10.30 and median OS = 30.63 months, p<0.001).
    CONCLUSION: Our findings highlight that immunohistochemical expression of SLFN11 and the density of TILs may serve as predictive biomarkers for chemotherapy response and survival in ovarian serous carcinoma, with potential implications for personalized treatment strategies.
    Keywords:  Schlafen 11 (SLFN11); Tumor-Infiltrating Lymphocytes (TILs); ovarian serous carcinoma; predictive biomarkers; survival
    DOI:  https://doi.org/10.31557/APJCP.2026.27.3.1123
  2. Int J Mol Sci. 2026 Mar 06. pii: 2431. [Epub ahead of print]27(5):
      Tumor-infiltrating lymphocytes (TILs) are an established predictor of pathological complete response (pCR) after neoadjuvant chemotherapy (NACT) in breast cancer. However, TILs primarily reflect the extent of immune infiltration and provide limited insight into immune functional state. We investigated whether integrating measures of immune infiltration (TILs), effector T-cell presence (CD8), and functional context (immune checkpoint components) may improve prediction of pCR beyond TILs alone. Pretreatment tumor biopsies from 166 patients with early breast cancer treated with standard NACT were assessed for stromal TILs and mRNA expression of CD8, PD-1, LAG-3, and TIM-3. Associations with pCR were evaluated using univariate and multivariable logistic regression, and composite immune phenotypes were constructed to capture functional immune states. In univariate analyses, higher TILs, CD8, PD-1, and LAG-3 were associated with pCR (all p < 0.05), whereas TIM-3 was not (p = 0.801). In multivariable models, TILs remained independently associated with pCR when adjusted for checkpoint markers, but this association was attenuated when CD8 was included, consistent with the strong biological correlation between TILs and CD8, and neither CD8 nor checkpoint markers retained independent significance. PD-1 and LAG-3 expression strongly correlated with CD8 and moderately correlated with TILs, indicating that checkpoint expression predominantly reflects an immune effector-engaged tumor microenvironment. Composite immune phenotypes based on CD8/PD-1 co-expression identified distinct immune functional states, with CD8-high/PD-1-high tumors demonstrating the highest pCR rates. Hierarchical modeling showed modest improvements in discrimination with sequential addition of immune variables to clinical predictors, with the integrative CD8/PD-1 model achieving the highest discrimination within the cohort (AUC = 0.849), although the magnitude of improvement beyond TIL assessment alone was limited. In conclusion, immune infiltration, effector T-cell presence, and functional immune context represent complementary dimensions for pCR prediction following NACT in breast cancer. However, TILs remain the most robust and clinically feasible immune biomarker.
    Keywords:  CD8-positive T cells; PD-1 immune checkpoint; breast cancer; immune microenvironment; neoadjuvant chemotherapy; pathological complete response; predictive biomarkers; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.3390/ijms27052431
  3. Front Immunol. 2026 ;17 1757366
      Ovarian cancer (OC), particularly high-grade serous ovarian cancer (HGSOC), is among the most lethal gynecologic malignancies, with its therapeutic challenges primarily stemming from a distinctly immunosuppressive tumor immune microenvironment (TIME). Neoadjuvant chemotherapy (NACT) has emerged as a crucial treatment strategy for advanced ovarian cancer; nevertheless, its impact on the tumor microenvironment-especially on tumor-infiltrating lymphocytes (TILs)-is not yet fully understood. As central mediators of antitumor immune responses, the density, composition, and dynamic changes of TILs are strongly associated with chemotherapy response and patient prognosis. Notably, spatial omics studies further revealed that, after NACT, a subset of CD8+ T cells can be confined within "myelonets" microdomains organized by myeloid cells, where interactions such as NECTIN2-TIGIT impose spatial restriction and induce functional exhaustion of T cells, thereby compromising their effective tumor killing. This review aims to systematically summarize the baseline characteristics and heterogeneity of lymphoid- and myeloid-derived TILs in ovarian cancer, elucidate the mechanisms underlying immune remodeling induced by NACT and their complex relationships with clinical outcomes, and further discuss combination therapeutic strategies and biomarker development based on dynamic TIL changes to enhance the clinical application of precision immunotherapy.
    Keywords:  biomarkers; immunotherapy; neoadjuvant chemotherapy; ovarian cancer; tumor immune microenvironment; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.3389/fimmu.2026.1757366
  4. Front Immunol. 2026 ;17 1771318
       Background: Biliary tract cancer (BTC) is a highly heterogeneous malignancy originating from the biliary epithelium or gallbladder mucosa, characterized by strong invasiveness and poor prognosis. Although surgery remains the primary curative strategy, most patients are diagnosed at advanced stages, limiting surgical opportunities. The traditional gemcitabine plus cisplatin chemotherapy regimen, although a standard treatment, has limited efficacy and often leads to drug resistance. In recent years, adoptive cell immunotherapy has emerged as a promising new avenue for BTC treatment.
    Main body: This review systematically elaborates on the research progress of various ACT strategies in BTC, including chimeric antigen receptor T cells, tumor-infiltrating lymphocytes, natural killer cells, cytokine-induced killer cells, and T-cell receptor-engineered T cells. Furthermore, it comprehensively analyzes current key challenges and discusses future directions and optimization strategies regarding these therapies.
    Conclusion: This review summarizes recent progress in adoptive cell therapy for biliary tract cancer and discusses optimization strategies to facilitate clinical translation.
    Keywords:  T-cell receptor-engineered T cells; adoptive cell immunotherapy; biliary tract cancer; chimeric antigen receptor T-cell therapy; cytokine-induced killer cells; natural killer cells; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.3389/fimmu.2026.1771318
  5. J Immunol Res. 2026 ;2026(1): e8444562
      Continuous antigen exposure initiates the developmental process of CD8+ T cell exhaustion, accompanied by a gradual increase in the expression of inhibitory receptors (IRs). Our previous study conceptualized T cell exhaustion as an over-activation status induced by chronic antigen stimuli. To intervene in the developmental process of CD8+ T cell exhaustion, we adjusted the over-activation status by intermittently blocking T cell activation signals with tacrolimus, a T cell activation inhibitor. Melanoma-bearing mice received intermittent tacrolimus (IT) and/or programmed cell death 1 (PD1) blockade antibody. Exhaustion phenotype of CD8+ tumor-infiltrating lymphocytes (CD8+TILs) was detected by flow cytometry. The expression levels of IRs (PD1 and CD223), as well as memory markers (Ly108 and CD127), were utilized to demarcate the extent of CD8+TILs exhaustion. Then, tyrosinase-related protein 2 peptide (Trp2180-188) was used to detect tumor-specific CD8+ TILs. Furthermore, tumor growth rate and tumor weight were also evaluated. We found that IT and/or PD1 blockade enhanced the infiltration of functional CD8+TILs. The findings demonstrated that both IT therapy and PD1 blockade enhanced the antitumor immunity. Combining IT and PD1 blockade led to a greater reduction in tumor growth rate and tumor weight. IT therapy also improved the response of CD8+TILs to melanoma-specific Trp2180-188 peptide. A detailed analysis of the CD8+TILs showed that Ly108 and CD127 reduced dramatically as the expression of PD1 increased. In comparison to PD1 blockade, combined treatment (IT plus PD1 blockade) significantly increased the number of intermediate IRs-expressing CD8+TILs, while reducing the number of high IRs-expressing CD8+TILs. These results indicated that combined treatment enhanced the function and decelerated the increase in IRs expression of CD8+TILs, deferring the developmental process of CD8+TILs exhaustion.
    Keywords:  PD1 blockade; T cell exhaustion; over-activation; tacrolimu
    DOI:  https://doi.org/10.1155/jimr/8444562
  6. Clin Cancer Res. 2026 Mar 12.
       PURPOSE: Brain metastasis (BM) is a deadly complication of systemic malignancy, which has been associated with defective cellular immunity. We sought to characterize the foundational elements and clinical relevance BM-associated immunosuppression using integrated molecular profiling in primary patient material.
    EXPERIMENTAL DESIGN: Retrospective patient tissue cohorts of breast (N=153) and lung (N=153) cancer BM were stratified by histopathological scoring of tumor-infiltrating lymphocytes (TILs) and clinical outcome, with a large subset of breast cancer samples further analyzed by T-cell receptor (TCR) and RNA sequencing. An ongoing clinical trial comparing pre-operative (pre-op) and post-operative (post-op) stereotactic radiosurgery (SRS)/stereotactic radiotherapy (SRT) in BM management was then leveraged to dissect radiation-induced immune responses by TCR and RNA sequencing.
    RESULTS: Patients with high-grade histopathological TIL infiltration and enriched TCR diversity demonstrated favorable prognoses in breast and lung cancer BM. Moreover, SRS/SRT treatment enhanced TCR diversity in the BM microenvironment, along with signatures of antigen processing and presentation. Finally, integrated analysis demonstrated that IR appeared to reactivate immune microenvironmental signatures normally suppressed in BM and upregulate immune signaling pathways correlated with favorable outcome in breast cancer BM patients.
    CONCLUSIONS: Our findings demonstrate that high TCR diversity in BM associates with favorable prognosis, pointing to therapeutically tractable targets within the immune microenvironment. Moreover, we show in a prospective clinical trial that IR enhances T cell-mediated immune responses, upregulating antigen-presentation and enhancing TCR diversity in BM. These results argue for increased therapeutic investigations of radiation-induced immunomodulatory effects in BM, potentially in association with immune checkpoint inhibition.
    DOI:  https://doi.org/10.1158/1078-0432.CCR-25-3525
  7. PLoS Med. 2026 Mar;23(3): e1004979
      Digitally automated spatial profiling of immune-tumor cell interactions using multispectral immunofluorescence holds promise as a biomarker to predict outcomes in early-stage breast cancer, but prospective validation and harmonization with existing biomarkers is necessary before clinical adoption.
    DOI:  https://doi.org/10.1371/journal.pmed.1004979
  8. Immunol Cell Biol. 2026 Mar 08.
      Chimeric antigen receptor (CAR) T cell therapies have shown remarkable efficacy in hematological malignancies, yet translation to solid tumors has been hindered by immunosuppressive tumor microenvironments, reduced T cell persistence and on-target/off-tumor toxicities. Constitutive CAR expression, typically driven by strong promoters such as EF1α, promotes tonic signaling, receptor clustering and antigen-independent activation, contributing to T cell exhaustion and adverse events. Inducible promoter systems have been proposed to improve control over CAR expression. NR4A1, a transcription factor (TF) activated during early T cell receptor (TCR) signaling, governs pathways central to T cell activation and dysfunction, making its promoter an attractive candidate for conditional CAR regulation. We compared constitutive (EF1α), synthetic inducible (6NFAT-NFκB and 2NFAT-2NurRE) and NR4A1 promoters to drive expression of a second-generation FRP5-CAR. NR4A1-driven CARs demonstrated low basal expression that was rapidly induced upon antigen encounter, reaching levels equivalent to EF1α-driven CARs while showing minimal antigen-independent signaling. Functionally, NR4A1-driven CARs mediated potent tumor lysis, preserved a less exhausted (PD-1low and TIM-3low) and more memory-like phenotype (CD62Lhigh and CD45RAhigh), and sustained robust antitumor responses in vitro and in vivo. These findings establish the NR4A1 promoter as a native, activation-inducible system to fine-tune CAR expression, while maintaining therapeutic efficacy comparable to constitutively expressed CAR T cells. This strategy provides a promising framework for advancing CAR T cell therapies against solid tumors.
    Keywords:  CAR T cells; PD1; T cell exhaustion; inducible promoters
    DOI:  https://doi.org/10.1111/imcb.70095
  9. Asian Pac J Cancer Prev. 2026 Mar 01. pii: 92101. [Epub ahead of print]27(3): 1061-1068
       BACKGROUND: Cervical cancer remains a major cause of mortality in low- and middle-income settings. We assessed whether two PIK3CA single-nucleotide polymorphisms (SNPs) rs6443624 (A/C) and rs141178472 (C/T) are associated with disease risk, clinicopathological features, and survival.
    MATERIALS AND METHODS: In a prospective case control study at a tertiary center, 154 participants were enrolled (77 cases, 77 controls). Genomic DNA was isolated from FFPE cervical tumors (QIAamp DNA FFPE Tissue Kit) and genotyped using TaqMan allelic discrimination. Clinicopathological variables (FIGO stage, histology, grade, treatment, tumor-infiltrating lymphocytes [TILs]) were abstracted from records. Genotype distributions were compared by Pearson chi-square. Associations with clinicopathological features used chi-square/Fisher's exact as appropriate; ANOVA compared age across genotypes. Overall survival (OS) was estimated by Kaplan-Meier and compared with the log-rank test; mean OS with SE and 95% CI is reported.
    RESULTS: Cases were predominantly locally advanced at presentation and squamous histology; most were moderately differentiated. rs6443624 differed significantly between cases and controls (χ²=21.1, p<0.001), with CC over-represented in cases and CA less frequent. rs141178472 showed no significant case control difference (χ²=2.9, p=0.086). For OS, rs6443624 showed a significant genotype effect (log-rank χ²=23.45, p=0.001): AA had the poorest survival, CA the longest, CC intermediate. rs141178472 was not associated with OS (χ²=1.06, p=0.588). Genotype clinicopathological correlations for stage group, grade, TILs, and treatment were non-significant or inconsistent, with some comparisons limited by small sample sizes.
    CONCLUSION: The PIK3CA rs6443624 variant appears to influence both susceptibility and prognosis in cervical cancer, highlighting its potential as a biomarker for molecular risk stratification. Validation in larger, multi-center cohorts incorporating HPV/p16 assessment and extended follow-up is warranted to confirm its clinical relevance.
    Keywords:  Cervical cancer; PIK3CA; Single-nucleotide polymorphism; rs6443624
    DOI:  https://doi.org/10.31557/APJCP.2026.27.3.1061
  10. BMC Cancer. 2026 Mar 13.
      
    Keywords:  Breast cancer; Estrogen receptor; Fractionation; Immune cells; Radiotherapy; Randomized; Recurrence; Survival; Tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.1186/s12885-026-15859-w
  11. Cancer Biol Med. 2026 Mar 10. pii: j.issn.2095-3941.2025.0645. [Epub ahead of print]23(2):
      The immune checkpoint blockade (ICB) approach in cancer therapy involves the disruption of immune checkpoint inhibitory signals on tumor-specific CD8+ T cells, thereby reinstating the immune activity of CD8+ T cells and yielding therapeutic efficacy. However, due to the co-expression of immune checkpoint molecules, such as CTLA-4 and PD-1 on tumor-infiltrating Tregs (TI-Tregs) and conventional T cells (Tconvs), immune checkpoint inhibitors (ICIs) inadvertently amplify the immunosuppressive activity of Tregs while targeting CD8+ T cells, which contributes to the failure of immune therapy. Conventional strategies targeting Tregs, including ICI/conventional kinase and chemokine/chemokine receptor blockade, generally induce systemic Treg depletion, which triggers autoimmune diseases. Thus, achieving high selectivity and specificity in targeting TI-Tregs is of paramount importance in mitigating adverse immunologic reactions. Targeting metabolism-based TI-Tregs has been shown to enhance target precision, providing potential for the development of adjunctive immunotherapeutic strategies. This article explores the reciprocal interaction between TI-Tregs and the tumor microenvironment (TME), elucidating metabolic reprogramming, while envisioning plausible high-selectivity targets for TI-Tregs without compromising systemic immune homeostasis and immune reactivity of effector T cells.
    Keywords:  CD8+ T cells; Tumor-infiltrating regulatory T cells; immune checkpoint inhibitors; immunometabolism; tumor microenvironment
    DOI:  https://doi.org/10.20892/j.issn.2095-3941.2025.0645
  12. Cell Rep Med. 2026 Mar 09. pii: S2666-3791(26)00075-3. [Epub ahead of print] 102658
      Solid tumors impose coupled stromal and immunologic barriers that limit T cell infiltration and function. Here, we engineer Salmonella VNP20009 to express gas vesicles (GVs), creating an intratumoral cavitation source that converts low-intensity focused ultrasound (LIFUS) into localized mechanical forces. LIFUS-activated GVs remodel the tumor microenvironment by reducing cancer-associated fibroblast (CAF) abundance, decompressing the matrix, and selectively disrupting CAF-CD8+ T cell communication via a mechanosensitive Notch1-Jagged1 axis. Single-cell RNA sequencing reveals a redistribution of CD8+ T cell states, characterized by enrichment of cytotoxic effector populations and attenuation of NOTCH signaling in memory-associated cells. These biomechanical changes enhance intratumoral CD8+ T cell infiltration and restore effector cytokine production. Leveraging this mechanism, we develop a mechano-priming approach for adoptive T cell therapies. Pre-conditioning with LIFUS-driven GVs improves CD8+ T cell cytotoxicity, strengthens tumor cell adhesion, reduces exhaustion signatures, and achieves durable tumor control and extended survival in orthotopic and metastatic models.
    Keywords:  NOTCH pathway; immunotherapy; mechanotransduction; tumor microenvironment; ultrasound
    DOI:  https://doi.org/10.1016/j.xcrm.2026.102658
  13. Adv Sci (Weinh). 2026 Mar 12. e74807
      CD8+ T cells are central executors of antitumor immunity, yet their activation, effector differentiation, and long-term persistence are governed by diverse post-translational modifications (PTMs). These chemical modifications function as rapid and reversible regulators that link antigenic stimulation, metabolic availability, and inflammatory cues to the transcriptional and chromatin programs that define CD8+ T cell fate. Core PTM classes-including phosphorylation, ubiquitination, acetylation, methylation, and glycosylation-precisely tune signaling thresholds, cytotoxic commitment, and memory formation, while emerging metabolism-responsive modifications such as lactylation directly connect nutrient flux to functional fitness. In solid tumors, chronic antigen exposure, hypoxia, nutrient restriction, and lactate accumulation profoundly remodel these modification networks, stabilizing dysfunction-associated states, impairing metabolic flexibility, and diminishing cytotoxic capacity. This review integrates current mechanistic understanding of how major PTM pathways coordinate the lifecycle of CD8+ T cells-from initial activation to effector acquisition, memory establishment, dysfunction, and exhaustion. We further discuss how the tumor microenvironment reprograms PTM landscapes to reinforce dysfunction and promote immune escape. Finally, we highlight the challenges and future directions in deciphering and targeting PTMs in CD8+ T cells. Future efforts to manipulate PTMs hold significant potential to improve cancer immunotherapies by restoring the antitumor efficacy of CD8+ T cells within the tumor microenvironment.
    Keywords:  CD8+ T cell; PTMs; TME; metabolic regulation; tumor immunotherapy
    DOI:  https://doi.org/10.1002/advs.74807
  14. J Clin Invest. 2026 Mar 10. pii: e195021. [Epub ahead of print]
       BACKGROUND: Immune checkpoint inhibitors (ICIs) targeting the programmed cell death-1 axis have revolutionized metastatic non-small cell lung cancer (mNSCLC) treatment. However, disease progression remains a concern, and the role of the complex tumor microenvironment (TME) in treatment failure is not fully understood.
    METHODS: In this biomarker study involving 103 patients with mNSCLC-including 81 patients who received ICI treatment-we evaluated the association between heterogeneous immune cell subsets and ICI efficacy through single-cell spatial profiling of pretreatment tumor tissue, using a 29-marker multiplex immunohistochemistry platform built for in-depth dissection of the TME.
    RESULTS: Among various types of intratumoral lymphocytes including T-helper 1 cells, regulatory T cells, and natural killer cells, only CD8+ T cells (TILs) were associated with ICI efficacy. Computational tissue segmentation underscored the importance of direct physical interactions between CD8+ TILs and cancer cells for ICI efficacy. TIL phenotyping identified CD39/CD103/Ki-67 positivity as a hallmark of exhausted yet functional tumor-reactive CD8+ TILs. Immunosuppressive tumor-associated macrophages (TAMs) and cancer-associated fibroblasts were independent unfavorable adversaries. High CD73 expression on cancer cells was suggested to confer tolerance to ICI in EGFR/ALK-oncogene+ NSCLC, potentially through M2-TAM accumulation and aberrant angiogenesis.
    CONCLUSION: Our study delineates the clinical relevance of heterogeneous immune cell subsets in ICI-treated mNSCLC, aiding the development of targeted therapeutic strategies.
    TRIAL REGISTRATION: Not applicable because this is a retrospective study.
    FUNDING: Osaka Cancer Society, KANAE Foundation for the Promotion of Medical Science, SGH Foundation, and YOKOYAMA Foundation for Clinical Pharmacology.
    Keywords:  Biomarkers; Cancer immunotherapy; Clinical Research; Immunology; Lung cancer; Oncology
    DOI:  https://doi.org/10.1172/JCI195021
  15. Cancer Res. 2026 Mar 11.
      The recent FDA approval of the first T cell receptor-engineered T (TCR-T) cell cancer therapy has solidified the treatment as a viable therapeutic strategy. However, only a fraction of patients who received this treatment achieved substantial and long-lasting responses, highlighting the need to understand the molecular underpinnings of these responses and develop more effective strategies to improve this therapy. Previous research has demonstrated that the activation of MyD88 signaling in tumor-specific T cells functions as a robust costimulatory signaling pathway that promotes effective antitumor T cell responses. Here, we developed a strategy for improving TCR-T cell therapies by creating a synthetic TCR in which the intracellular domain of CD3ζ and a modified MyD88 are appended to the β-chain of a tumor-reactive TCR. The β:CD3ζ:MyD88 TCR activated MyD88 signaling in a tumor-antigen/TCR-specific manner, and β:CD3ζ:MyD88 TCR-T cells exhibited enhanced functionality and a reduced propensity to become exhausted. Furthermore, MyD88 signaling promoted T cell persistence and expansion in vitro. In vivo, tumor-infiltrating β:CD3ζ:MyD88 TCR-T cells skewed the immunosuppressive tumor microenvironment toward a less immunosuppressive state. Finally, β:CD3ζ:MyD88 TCR-T cells substantially delayed tumor growth kinetics in a melanoma model. These findings introduce an approach for improving TCR-dependent T cell responses by directly appending signaling domains to the full-length TCR and exemplify the utility of activating MyD88 signaling in tumor-specific T cells.
    DOI:  https://doi.org/10.1158/0008-5472.CAN-25-0777
  16. Clin Exp Med. 2026 Mar 08.
      Multiple myeloma (MM) is a heterogeneous hematologic cancer marked by clonal plasma cell expansion in the bone marrow. Although treatments have improved, relapse remains common due to clonal evolution, tumor microenvironment changes, ultimately leading to drug resistance. This study utilized single-cell RNA sequencing data analysis to explore immune microenvironment dynamics during MM progression and relapse, aiming to uncover key pathways and cellular interactions correlated with disease relapse. ScRNA-seq data from 20 MM patients (10 primary, 2 remission, 8 relapsed) from the GEO dataset GSE223060 were analyzed. After quality control and batch correction, cells were clustered and annotated. Differential gene expression and functional enrichment analyses were conducted to explore cellular functions. Pseudotime analysis was used to trace plasma cell differentiation, and cell-cell communication was analyzed. Immunohistochemistry and flow cytometry were used for validation.60,234 high-quality single cells were classified into 12 distinct populations. Relapsed MM showed increased T cell infiltration and decreased plasma cells. Relapsed samples had more regulatory T cells (Tregs) and impaired CD8 + T cells. MIF was identified as a key regulator in plasma cell evolution, linked to B cell receptor and interferon-alpha signaling. Enhanced MIF pathway activity was noted between plasma cells and CD8 + T cells in relapsed MM. Increased MIF expression was confirmed in relapsed tissues. Our findings reveal profound immune microenvironment remodeling in relapsed MM, characterized by MIF-mediated signaling, NF-κB suppression, and CD8⁺ T cell dysfunction. These results provide new insights into the mechanisms of MM relapse and highlight potential therapeutic targets for preventing disease relapse.
    Keywords:  Immune microenvironment; MIF; Multiple myeloma; NF-κB; Relapse; Single-cell RNA sequencing
    DOI:  https://doi.org/10.1007/s10238-026-02113-7
  17. Immune Netw. 2026 Feb;26(1): e13
      Chimeric antigen receptor (CAR)-T cell therapy has achieved substantial clinical success in hematological malignancies and has become a key modality in cancer immunotherapy. However, the current ex vivo autologous manufacturing model continues to face high costs, complex logistics, and prolonged production timelines, which collectively limit scalability and patient accessibility. Direct in vivo CAR-T generation could overcome these bottlenecks by bypassing ex vivo manipulation, but systemic administration must address significant safety and efficacy hurdles. In this review, we summarize core principles of lentiviral vector design, including essential genomic elements and the evolution of safety-enhanced, third-generation self-inactivating vector system. We then discuss emerging bioengineering strategies to optimize in vivo gene delivery, including pseudotype engineering for T cell targeting, immune-evasion strategies, transgene/payload engineering, and genetic armoring to enhance therapeutic performance and safety. Finally, we review the current clinical landscape and highlight early evidence supporting the feasibility of in vivo CAR-T generation from ongoing clinical-stage programs. Collectively, these advances are accelerating the maturation of in vivo CAR-T platforms toward scalable modalities with the potential to substantially broaden access to advanced cellular immunotherapies.
    Keywords:  Gene transfer techniques; Genetic vectors; Immunotherapy; In vivo CAR-T; Lentivirus
    DOI:  https://doi.org/10.4110/in.2026.26.e13
  18. Front Immunol. 2026 ;17 1764549
      The identification of stem-like CD8+ T cells, also termed progenitor or precursor of exhausted T cells (TPEX), has reshaped our understanding of durable antitumor immunity. These cells exhibit progenitor-like properties, including self-renewal capacity and multilineage differentiation potential, giving rise to both effector-like and terminally exhausted CD8+ T cell subsets. Accordingly, the abundance of stem-like CD8+ T cells correlate strongly with improved clinical outcomes in patients receiving immune checkpoint inhibitors, adoptive cell therapy, or cancer vaccines across multiple tumor types. This review synthesizes recent advances in TPEX cells biology, highlighting interconnected research pillars, including: specialized niche microenvironments that sustain stemness of TPEX cells through coordinated chemokine signaling and antigen-presenting cell interactions; core molecular circuitry that dynamically balances self-renewal versus effector differentiation via transcription factors and cytokines; and therapeutic reprogramming strategies that harness TPEX cells as the primary driver of immunotherapy efficacy. Further, we explore strategies to augment the functionality of TPEX cells through niche modulation, stem-like CAR-T engineering, and combinatorial approaches, highlighting the trend that targeting TPEX cells thus emerge as a transformative future strategy to overcome immunotherapy resistance and achieve a durable response.
    Keywords:  cancer immunotherapy; self-renewability; stem-like T cells; therapeutic implications; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2026.1764549
  19. Cancer Lett. 2026 Mar 09. pii: S0304-3835(26)00180-1. [Epub ahead of print]646 218417
      Though cancer immunotherapy has revolutionized the treatment of several tumor types, progress for immunotherapy in gastrointestinal (GI) tumors has been difficult. Recently, there have been rapid developments in bispecific T-cell engagers for the treatment of several hematologic malignancies. These can circumvent several limitations of conventional cancer immunotherapy by using bispecific antibodies to target CD3 and a tumor-specific antigen, thereby promoting anti-tumor cytotoxicity independent of major histocompatibility complex restriction or T-cell receptor specificity. Given the significant efficacy of this approach in leukemia, myeloma, and lymphoma, there is great interest in the potential for bispecific T-cell engagers in GI cancers. Here, we provide a comprehensive summary of current clinical and preclinical studies exploring bispecific T-cell engagers in GI cancers. Further, we briefly discuss potential barriers to therapeutic efficacy and important considerations regarding potential toxicity.
    Keywords:  Bispecific T-cell engager; Gastrointestinal cancer; Immunotherapy; Tumor immunology
    DOI:  https://doi.org/10.1016/j.canlet.2026.218417
  20. Immunother Adv. 2026 ;6(1): ltag004
       Introduction: Programmed cell death protein 1 (PD-1) inhibitors improve survival in advanced melanoma but can induce immune-related adverse events (irAEs). IrAEs have been linked to better outcomes. However, it remains unclear whether specific irAE types drive this effect and how corticosteroid treatment of irAEs influences survival.
    Materials and methods: A seven-year retrospective cohort study of 301 patients with advanced cutaneous melanoma treated with single-agent PD-1 inhibition at Sahlgrenska University Hospital. irAEs were identified using CTCAE v4.0/v5.0, and irAEs requiring systemic corticosteroids or endocrine replacement therapy were included. Corticosteroid therapy was categorized as low dose (≤0.5 mg/kg prednisolone equivalent) or high dose (>0.5 mg/kg). Overall survival (OS) was assessed using Kaplan-Meier and Cox models, including time-dependent analyses to address immortal time bias.
    Results: Patients with irAE (109 of 301 patients) had longer OS than those without irAEs. Of the eight most common irAEs, four were associated with superior survival, one was borderline significant, and three were non-significant. Rheumatic irAEs and late-onset thyroid irAEs remained associated with improved OS after adjustment for negative prognostic factors and immoral time bias. Colitis irAE were borderline significant in univariate analysis. Sarcoidosis-like and hypophysitis irAEs were rare but conferred excellent outcomes. Hepatitis, nephritis, and pneumonitis were not associated with better survival. Most survival-associated irAEs were treated with a lower start dose of corticosteroids but duration and time to onset were similar to non-survival-associated irAEs.
    Conclusion: Rheumatic, endocrine, and sarcoidosis-like irAEs are markers of superior survival and suggest that lower initial corticosteroid doses may preserve PD-1 inhibitor efficacy.
    Keywords:  PD-1 inhibitor; immune-related adverse events; melanoma; survival
    DOI:  https://doi.org/10.1093/immadv/ltag004