bims-tuinly Biomed News
on Tumor-infiltrating lymphocytes therapy
Issue of 2026–05–03
27 papers selected by
Pierpaolo Ginefra, Ludwig Institute for Cancer Research



  1. Anticancer Res. 2026 May;46(5): 2387-2401
       BACKGROUND/AIM: Colorectal cancer (CRC) remains the leading cause of cancer-related mortality worldwide and necessitates the development of novel therapeutic strategies. The tumor immune microenvironment (TME) critically influences disease progression and the response to immune checkpoint inhibitors (ICIs). Tumor-infiltrating lymphocytes (TILs) are key components of the TME with established prognostic and predictive significance. Nevertheless, detailed TIL characterization using flow cytometry has not been fully investigated in CRC.
    MATERIALS AND METHODS: We analyzed TILs from 90 fresh CRC specimens using multicolor flow cytometry to investigate the association between specific T cell subsets and clinical outcomes. Patients were classified into Hot and Cold groups based on hierarchical clustering of TIL marker expression.
    RESULTS: The Hot group demonstrated significantly better overall survival (OS) compared to the Cold group (5-year OS: 86.7% vs. 63.9%, p=0.006), although recurrence-free survival (RFS) was not significantly different (5-year RFS: 79.5% vs. 66.1%, p=0.24). CITRUS analysis revealed that PD-1+Tim-3+CD103+CD8+ T cells were enriched in hot tumors (32.1% vs. 6.1%, p<0.001) and correlated with a favorable prognosis. Importantly, multivariate analysis demonstrated that a low frequency of PD-1+Tim-3+CD103+ cells among CD8+ T cells was an independent prognostic factor for OS [hazard ratio (HR)=3.36, 95% confidence interval (CI)=1.20-9.34, p=0.02].
    CONCLUSION: A high frequency of PD-1+Tim-3+CD103+ CD8+ T cells is associated with better survival in CRC, highlighting their potential as a prognostic biomarker and therapeutic target.
    Keywords:  CD103; PD-1; Tim-3; Tumor-infiltrating lymphocytes; colorectal cancer; tumor microenvironment
    DOI:  https://doi.org/10.21873/anticanres.18125
  2. Cell. 2026 Apr 29. pii: S0092-8674(26)00226-6. [Epub ahead of print]
      Tumor-infiltrating lymphocytes (TIL) often fail to restrain tumor growth due to progressive differentiation into an "exhausted" state. Tissue-resident memory T cells (TRM) maintain protection from infection for years in healthy tissues, and patient tumors that contain TIL with TRM features are associated with better prognosis. Proteomic and transcriptomic profiling of T cell populations identified proteostasis as a significant factor distinguishing TRM and progenitor-exhausted TIL from terminally exhausted TIL, including loss of E3 ubiquitin ligases NEURL3, RNF149, and WSB1, with accumulation of unfolded proteins despite functional proteasome activity. Enforced expression of these ligases in T cells preserved stem-like TCF1+ populations and improved function in tumors and chronic infection, whereas deficiency impaired TIL and altered T cell differentiation during acute infection. Sustained ligase expression rescued the accumulation of unfolded proteins in TIL and improved immunotherapy outcomes in preclinical models, underscoring the critical role of proteostasis in TIL function and highlighting a promising avenue for advancing cancer immunotherapy.
    Keywords:  CD8(+) T cell; E3 ubiquitin ligase; T cell exhaustion; cancer; immunotherapy; proteostasis; tumor; tumor-infiltrating lymphocyte
    DOI:  https://doi.org/10.1016/j.cell.2026.02.019
  3. bioRxiv. 2026 Apr 19. pii: 2026.04.15.718702. [Epub ahead of print]
      Survival outcomes for pediatric Burkitt lymphoma (BL) substantially vary depending on geography (50-90%), which also serves as a proxy for the prevalence of Epstein-Barr virus (EBV) within the tumors. Although BL is considered an immunologically "cold" tumor with few tumor-infiltrating lymphocytes (TILs), their functional status has not been fully evaluated, especially for EBV-positive disease. Here, we characterize the exhaustion and activation profiles of T cells in the tumor microenvironment (TME) of EBV-positive BL using orthogonal methods, single-cell gene expression analysis, spectral flow cytometry, and immuno-histochemistry staining (IHC). We found that CD8+ TILs displayed a mosaic of immune inhibitory gene expression encoding, PD1, TIGIT, LAG3 and HAVCR2/TIM3. IHC validated the expression of PD1 and TIGIT on CD8+ TILs, as well as their respective ligands, PDL-1, PVR, and Nectin-2 on malignant B cells. Despite exhaustion-associated signatures, CD8+ TILs retain cytotoxic potential, expressing granules (i.e. Granzyme A, Perforin) and cytokines (i.e. IFNγ) and demonstrate an increased uptake of metabolites such as glucose, arginine, and methionine. In peripheral blood, pediatric BL patients exhibited a significantly higher abundance of PD1+TIGIT+ CD8+ T cells compared to healthy children. Notably, these circulating T cells from BL patients express significantly lower levels of TOX, suggesting they are not irreversibly dysfunctional. Together, our results indicate that CD8+ T cells both in the TME and in circulation of children with BL are not terminally exhausted but remain poised for functional re-invigoration. These findings support the potential integration of immune checkpoint inhibitors into combination chemotherapeutic regimens to improve outcomes for these children.
    DOI:  https://doi.org/10.64898/2026.04.15.718702
  4. Cureus. 2026 Mar;18(3): e105981
      Background and objective Glial tumors are increasingly recognized as immunologically active neoplasms in which macrophage-rich and lymphocyte-poor microenvironments may influence aggressiveness. Cluster of differentiation 163 (CD163) highlights tumor-associated macrophages, whereas CD8 marks cytotoxic tumor-infiltrating lymphocytes (TILs). This study aimed to evaluate CD163 expression and CD8-positive TILs in glial tumors and examine their association with tumor grade. Methods This cross-sectional study included 50 histopathologically confirmed glial tumors. Immunohistochemistry for CD163 and CD8 was performed on formalin-fixed paraffin-embedded tissue sections. CD163 was scored as absent, weak, moderate, or strong, and CD8 infiltration was categorized as low or high. Associations with World Health Organization (WHO) tumor grade and histologic aggressiveness were analyzed using the chi-square test, Fisher's exact test, and Spearman's correlation. Results The mean age of the cohort was 42.7 ± 16.1 years, with males accounting for 29/50 (58.0%) and females for 21/50 (42.0%). High-grade gliomas comprised 32/50 (64.0%) cases, while low-grade tumors accounted for 18/50 (36.0%); grade IV tumors were the largest subgroup (20/50, 40.0%). CD163 positivity was observed in 40/50 (80.0%) tumors and increased significantly with tumor grade (rho = +0.59, p < 0.001). CD163 positivity was more frequent in high-grade than in low-grade tumors (30/32 (93.8%) vs. 10/18 (55.6%), p = 0.004). High CD8 infiltration was seen in 15/50 (30.0%) tumors and low CD8 infiltration in 35/50 (70.0%), with CD8 levels declining significantly with increasing grade (rho = -0.33, p = 0.021). Strong CD163 expression with low CD8 infiltration was present in 17/50 (34.0%) tumors and was significantly associated with high-grade lesions (16/32 (50.0%) vs. 1/18 (5.6%), p = 0.004). Moderate-to-strong CD163 expression was associated with necrosis (18/20 (90.0%), p = 0.009) and microvascular proliferation (16/18 (88.9%), p = 0.024). Conclusions Higher-grade glial tumors demonstrate a macrophage-dominant and CD8-restricted immune microenvironment. Combined assessment of CD163 and CD8 may serve as a practical indicator of aggressive tumor biology in routine diagnostic practice.
    Keywords:  cd163; cd8; glial tumors; glioma; immunohistochemistry; tumor microenvironment; tumor-associated macrophages; tumor-infiltrating lymphocytes; who grade
    DOI:  https://doi.org/10.7759/cureus.105981
  5. Oncoimmunology. 2026 Dec 31. 15(1): 2658916
      BET inhibitors (BETi) have shown potential to augment tumor immunogenicity in melanoma. However, conflicting evidence exists regarding their precise mechanism of action, and their overall impact on melanoma immunogenicity and antitumoral T cell responses remains unclear. To address this, human melanoma cell lines treated with JQ1 and/or IFNγ were investigated for gene and protein expression changes in key pathways governing immunogenicity and cocultured with autologous tumor-infiltrating lymphocytes (TIL) with known antigen-specificity. JQ1-induced proteome-wide alterations were examined using mass spectrometry-based cellular thermal shift assay (MS-CETSA), which revealed that JQ1 broadly impacts melanoma immunogenicity by regulating IFN signaling, antigen processing and presentation, and innate immune signaling pathways. More specifically, JQ1 enhanced JAK1/STAT1 signaling and upregulated components of the HLA class I (HLA-I) antigen processing and presentation machinery (APM), increased MART-1 expression while concomitantly dampening tumoral expression of PD-L1, IDO1, and HLA class II (HLA-II). Functionally, JQ1 markedly improved tumor recognition by autologous MART-1- and neoantigen-specific CD8+ TIL, while dampening CD4+ TIL activation through the downregulation of Cathepsin S (CTSS). Preliminary results using JQ1-treated melanoma cells in a mixed lymphocyte-tumor cell culture (MLTC) markedly enhanced TIL proliferation and resulted in a T cell product enriched for CD8+ T cells. These findings reveal how the pleiotropic effects of BETi on melanoma cells broadly boost their immunogenicity towards CD8+ T cells and uncover novel pathways that might be therapeutically exploited to enhance CD8+ T cell-mediated anti-tumor immunity in ex vivo and in vivo approaches to cancer immunotherapy.
    Keywords:  Cancer immunotherapy; bromodomain and extra-terminal inhibitors; immune escape; tumor immunogenicity; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.1080/2162402X.2026.2658916
  6. Res Sq. 2026 Mar 13. pii: rs.3.rs-8941883. [Epub ahead of print]
      Most antitumor CD8 ⁺ T cells in patients exhibit dysfunctional phenotypes, limiting the efficacy of adoptive cell transfer (ACT) against cancer. Although cancer vaccines can induce antitumor stem-like T cell (T SL ) phenotypes, whether they can reverse T cell dysfunction during ACT remains unclear. Using murine neoantigen-specific tumor models, we show that concurrent neoantigen-vaccination enhances the antitumor activity of ACT-products dominated by dysfunctional T cells, relying on host antigen-presenting cells. Vaccination remodels the immunosuppressive tumor microenvironment and promotes the expansion of T SL cells into tumors and lymphoid organs. Mechanistically, vaccination does not directly rescue dysfunctional T cells; but selectively amplifies low-frequency T SL (as low as 0.1% in infusion) to mediate tumor control. Analysis of human dysfunctional TIL-ACT infusion products containing scarce antitumor T SL cells (~1%) administered to a patient with metastatic melanoma corroborated these findings, demonstrating complete clinical tumor regression and expansion of adoptively transferred tumor-specific-TIL clonotypes only after vaccination. These data suggest that concurrent vaccines can unlock the therapeutic potential of rare stem-like T cells within otherwise ineffective dysfunctional ACT.
    DOI:  https://doi.org/10.21203/rs.3.rs-8941883/v1
  7. Biology (Basel). 2026 Apr 13. pii: 614. [Epub ahead of print]15(8):
      Glioblastomas (GBMs) are the most aggressive form of brain cancer recalcitrant to both current standard-of-care and immune checkpoint therapies that benefit other cancer patients. Adoptive cell therapies (ACT) using patients' own immune cells have long been explored as a treatment strategy, including the historically studied lymphokine-activated killer (LAK) cells, the evolving chimeric antigen receptor (CAR) directed immune cells, the newly emerging tumor-infiltrating T lymphocyte (TIL) therapies, and others. Preclinical and clinical studies have shown promise but also highlighted significant challenges. In this review, we summarize these findings, highlight recent developments, discuss current limitations, and emphasize how ACT may benefit from contemporary and future insights into the co-evolution of TILs with other cells within the GBM tumor microenvironment (TME).
    Keywords:  CAR-T; adoptive cell therapy; glioblastoma; tumor microenvironment; tumor-infiltrating lymphocyte
    DOI:  https://doi.org/10.3390/biology15080614
  8. Breast Cancer Res. 2026 Apr 26.
      
    Keywords:  Associated fibroblast; Cancer; Immunotherapy; Infiltrating lymphocyte; Negative breast cancer; Triple; Tumor; Tumor immune microenvironment
    DOI:  https://doi.org/10.1186/s13058-026-02285-w
  9. Transplant Cell Ther. 2026 Apr 25. pii: S2666-6367(26)00319-2. [Epub ahead of print]
       BACKGROUND: Tumor infiltrating lymphocyte (TIL) therapy entails isolating, activating, expanding, and reinfusing isolated lymphocytes from tumors, presumably representing a collection of high affinity T cells that can recognize the melanoma tumor specific peptides expressed on endogenous HLA antigens. FDA recently approved Commercial TIL (Lifileucel; Amtagvi®), for treatment of BRAF wild type/resistant, checkpoint inhibitor failure, unresectable or metastatic melanoma, based on registrational trial showing an overall response rate of 31.5% in treated patients. Following FDA approval, patient outcomes beyond the originally selected clinical trial populations remain unknown.
    OBJECTIVE: We report initial real-world, single institutional observations and outcomes with melanoma referred for TIL therapy.
    METHODS: Retrospective analysis of cell therapy database of outcomes in 45 patients with unresectable or metastatic melanoma referred for TIL therapy considerations are reported.
    RESULTS: The median age was 68 years (27-83),37 (82.2%) had stage IV and 38 (84.4%) had BRAF wild-type disease, and 15 (33.3%) had CNS disease. 23 patients were male (51.1%), 28 (62.2%) patients completed surgical tumor harvest, 23(51.1%) patients completed TIL infusion, and 1 patient was just starting LD chemotherapy at the time of data analysis. 3 patients died from disease progression, and one went on comfort care prior to starting lymphodepleting chemotherapy. 8 (28.5%) TIL products were out of specification. 17 referred patients did not proceed to tumor resection: 8 (47.1%) were deemed ineligible due to small tumor size (<1.5 cm), co-morbidities or nonresectable site/brain mets,3 had not definitive evidence of disease, 2 died due to rapid disease progression, 3 deferred due to autoimmune colitis from prior CPI, and pt choice (n=1). The median overall survival for all patients who successfully pursued TIL therapy was not reached with 1-year OS of 79.2% (95% CI 60.2% to 100%) compared to patients who did not pursue TIL therapy with a mOS of 10.15 months and with 1-year OS of 42% (95% CI 23.4% to 75.4%) [p 0.007] (Fig. 2). Workflow modifications were implemented as part of a quality improvement initiative after six months. Upon receipt of a TIL referral, consultation with the Cellular Therapy (CT) team was initiated, followed by an urgent referral to Surgical Oncology. A CT nurse served as the central point of contact, coordinating all subsequent encounters, including operating room scheduling, tumor collection, CT laboratory processing, and industry partner manufacturing slot allocation. Table 2 demonstrates a reduction of the average time interval between referral and CT consult (17.6 vs 10.7 days with the new workflow), and a time interval between initial referral and receiving actual TIL infusion (128 days vs 96.3 days).
    CONCLUSIONS: Our institutional real-world data show that only about half of TIL therapy referrals will proceed with the actual TIL infusions. While TIL therapy seeks to achieve the approximately 32% response rate observed in the registrational trial, real-world outcomes in an intent-to-treat population are anticipated to be inferior. Advanced melanoma affords a narrow time window from referral to completion of TIL manufacturing and infusion, necessitating efficient workflows to enable early treatment and optimize patient outcomes.
    Keywords:  BRAF inhibitors; Immune checkpoint inhibitors (ICI); Interleukin-2 (IL-2); Lymphodepleting chemotherapy (LD chemo); Melanoma; Tumor infiltrating lymphocyte (TIL) therapy
    DOI:  https://doi.org/10.1016/j.jtct.2026.04.032
  10. PeerJ. 2026 ;14 e21052
       Background: The immune microenvironment at the tumor invasion front plays a pivotal role in cancer progression. Tumor budding, an aggressive histopathological feature, has been linked to poor outcomes in various malignancies. However, its impact on the tumor immune microenvironment remains poorly understood. This retrospective study aimed to determine whether tumor budding is a risk factor for lymph node metastasis (LNM) in stage IB1 cervical squamous cell carcinoma (CSCC) and to explore the relationship between PD-L1 expression in tumor cells and CD8+ and FOXP3+ tumor-infiltrating lymphocytes (TILs) within tumor budding regions.
    Methods: Tumor budding was retrospectively evaluated in 106 cases of International Federation of Gynecology and Obstetrics (FIGO) (2009) stage IB1 CSCC. High-grade tumor budding was defined as ≥ 15 buds per 10 high-power fields (HPFs). Immunohistochemistry was used to detect PD-L1, CD8, and FOXP3 expression. CD8+ T cells and FOXP3+ regulatory T cells (Tregs) were quantified separately intraepithelial and stromal compartments.
    Results: High-grade tumor budding was identified in 48 cases (45.3%) and was significantly associated with lymph node metastasis (LNM) on univariate analysis; however, it was not an independent predictor of LNM on multivariable logistic regression analysis. PD-L1 expression was detected in 53.8% (57/106) of the cohort, with overexpression observed in tumor budding areas. Three distinct PD-L1 expression patterns were identified: diffuse, marginal/tumor budding (MT), and negative. Notably, tumors with MT PD-L1 expression exhibited more favorable clinicopathological features compared to those with diffuse PD-L1 expression, including smaller tumor size, well differentiation, and low-grade tumor budding. In terms of the tumor immune microenvironment, PD-L1-negative tumors exhibited sparse infiltration of CD8+ T cells and FOXP3+ Tregs, whereas tumors with the MT pattern showed abundant stromal infiltration of both cell types. In contrast, diffuse PD-L1 expression was associated with abundant stromal and intraepithelial infiltration of CD8+ T cells and FOXP3+ Tregs.
    Conclusions: High-grade tumor budding is associated with LNM in stage IB1 CSCC. Three distinct PD-L1 expression patterns within tumor budding areas are associated with clinicopathologic features and immune cell infiltration profiles. PD-L1 expression patterns may warrant further investigation as potential biomarkers for immunotherapy response.
    Keywords:  CD8; Cervix; FOXP3; Lymph node metastasis; PD-L1; Squamous cell carcinoma; Tumor budding
    DOI:  https://doi.org/10.7717/peerj.21052
  11. Sci Rep. 2026 Apr 30.
      Adoptive cell therapy (ACT) with tumor-specific CD8+ T cells (TSTs) induces tumor regression but rarely achieves durable responses in solid tumors. This limitation stems from secondary counter-regulatory mechanisms that are also induced by ACT, notably the recruitment of tumor-infiltrating myeloid cells (TIMs). However, the precise dynamics of these responses and the optimal TST dosing strategies to overcome their immunosuppression remain largely unclear. Here, we developed a mathematical model of ACT incorporating TIM-driven counter-regulation and simulated alternative TST dosing strategies based on data from B16F10 melanoma-bearing mice. Our models revealed that, compared with a single administration strategy, fractionated and response-guided dosing strategies reduced tumor burden by up to 83% while using about 40% fewer TSTs. These results were supported by transcriptomic analysis showing that ACT-induced TIMs initially exhibited pro-inflammatory traits but later shifted into suppressive states, suggesting that fractionated TST dosing could repeatedly induce their stimulatory potential. Together, our findings advance understanding of counter-regulatory mechanisms in ACT and highlight the potential of fractionated dosing as a rational strategy to overcome them.
    Keywords:  Adoptive cell therapy; CD8+ T cells; Computational biology; Mathematical model; Tumor microenvironment; Tumor-infiltrating myeloid cells
    DOI:  https://doi.org/10.1038/s41598-026-50922-3
  12. J Immunother Cancer. 2026 Apr 30. pii: e014822. [Epub ahead of print]14(4):
      Clinical trials of adoptive cellular therapy demonstrate that a key characteristic associated with durable responses is in vivo expansion and persistence of transferred T cells. Strategies to develop a less differentiated, stem/memory population in the infusion product and peri-infusional regimens to promote the maintenance of desired T cell states following adoptive transfer would be desirable. Endogenous T cell therapy studies have routinely achieved memory T cells enriched for expression of interleukin (IL)-7 receptor; to eliminate the conventional requirement for immunosuppressive lymphodepletion and its attendant life-threatening toxicities, we performed the first-in-human use of IL-7 in combination with adoptively transferred antigen-specific memory CD8 T cells in a patient with refractory metastatic uveal melanoma. Single-cell immune repertoire profiling of serial peripheral blood sampling revealed substantial in vivo proliferation and expansion of a stem cell memory population in the endogenous T cell therapy product that achieved a >79% predominance of total circulating T cells by 3 weeks post-infusion in this non-lymphodepleted recipient. Although the patient's disease ultimately progressed, these findings demonstrate safety and proof of concept for an IL-7 treatment regimen for expansion of adoptively transferred T cells in vivo and induced memory differentiation in a heavily pretreated patient with refractory solid malignancy.
    Keywords:  Adoptive cell therapy - ACT; Cytokine; Memory; T cell
    DOI:  https://doi.org/10.1136/jitc-2026-014822
  13. Sci Immunol. 2026 May;11(119): eadz0348
      Metabolic perturbations in the tumor microenvironment profoundly compromise the stemlike properties and effector functions of CD8 T cells. Deciphering the metabolic circuitry that sustains T cell stemness is critical for reinvigorating tumor-infiltrating lymphocytes and augmenting immunotherapeutic efficacy. Here, we identify citraconate, an itaconate isomer, as a metabolite markedly depleted in CD8 T cells subjected to chronic antigen stimulation or hypoxic conditions. Citraconate supplementation preserves stemlike characteristics, attenuates ferroptosis, and potentiates T cell-mediated antitumor immunity. Mechanistically, citraconate maintains intracellular cyclic adenosine monophosphate (cAMP) concentrations by suppressing phosphodiesterase1A/C (PDE1A/C) expression and preserving mitochondrial integrity, thereby activating protein kinase A (PKA) signaling. This activation transcriptionally represses arachidonate-5-lipoxygenase (ALOX5), consequently reducing arachidonic acid peroxidation. Clinically, diminished ALOX5 or PDE1A expression correlates with reduced T cell exhaustion and improved responses to immune checkpoint blockade (ICB) therapy. Our findings reveal the citraconate-mediated PDE1-cAMP-ALOX5 axis as a potential therapeutic target for enhancing cancer immunotherapy.
    DOI:  https://doi.org/10.1126/sciimmunol.adz0348
  14. J Transl Med. 2026 Apr 25. pii: 595. [Epub ahead of print]24(1):
      
    Keywords:  Coculture models; Immunotherapy; Tumor microenvironment (TME); Tumor organoids; Tumor-infiltrating lymphocytes (TILs); Vγ9Vδ2 T cells; γδ T cells
    DOI:  https://doi.org/10.1186/s12967-026-07706-0
  15. JCI Insight. 2026 Apr 28. pii: e203622. [Epub ahead of print]
      Tumor-infiltrating CD8 cells recognize neoantigens created by tumor-specific mutations. Nonetheless, even after checkpoint inhibitor therapy, most patients progress. A deeper understanding of anti-tumor responses could facilitate development of better therapies. To enable such studies, we applied TCXpress, a high throughput platform that clones fully expressible TCRs from single cells into retro- or lenti- viral vectors without sequencing or gene synthesis, to study TCRs from CD8 cells infiltrating mouse MC38 tumors. We expressed cloned TCRs in reporter cells and interrogated TCR specificity by coculturing them with B6WT3 cells transduced with tandem minigenes encoding predicted neoantigens. We isolated TCRs reactive against epitopes from mutant Rpl18, Adpgk, Psmd2, and Zc3h7b along with self-reactive TCRs that recognized normal B6 and MC38 cells. Importantly, we successfully treated MC38-bearing mice with T cells transduced with anti-Rpl18 TCRs. These results establish a system that could be used to study many types of T cell responses and validates a therapeutic approach that could be tested in the clinic.
    Keywords:  Cancer immunotherapy; Immunology; Immunotherapy; Oncology; T cell receptor
    DOI:  https://doi.org/10.1172/jci.insight.203622
  16. Clin Transl Radiat Oncol. 2026 Jul;59 101172
       Introduction: Despite widespread adoption of neoadjuvant chemoradiotherapy (nCRT), locally advanced rectal cancer (LARC) shows highly heterogeneous treatment responses and survival outcomes. Pretreatment biopsy-derived Immunoscore (ISB) and the pan-immune-inflammation value (PIV) reflect local and systemic inflammation, respectively, and each has demonstrated prognostic value in LARC. However, the prognostic impact of integrating ISB with PIV has not been evaluated. This study aimed to determine whether combining ISB and PIV to jointly assess local and systemic inflammatory profiles improves risk stratification in LARC.
    Materials and Methods: We retrospectively analyzed 65 patients with LARC who underwent nCRT and surgery. ISB was assessed using pretreatment endoscopic biopsy specimens immunohistochemically stained for CD3 and CD8.
    Results: Patients were stratified into three groups according to their combined PIV-ISB profiles: Group 1 (PIV-High and ISB-Low), Group 2 (mixed-risk patterns), and Group 3 (PIV-Low and ISB-Intermediate/High). Group 1 exhibited higher C-reactive protein levels than those of Group 3 (p = 0.043). Five-year overall survival (OS) rates were 44.4%, 78.1%, and 82.7% in Groups 1, 2, and 3, respectively (p = 0.007), whereas disease-free survival (DFS) did not differ significantly (p = 0.186). In multivariate analysis, Group 2 independently predicted OS (vs. Group 1; hazard ratio [HR] 0.190, 95% confidence interval [CI] 0.043-0.831, p = 0.027), while lymphovascular invasion predicted OS (HR 6.386, 95% CI 1.412-28.882, p = 0.016) and DFS (HR 3.683, 95% CI 1.272-10.664, p = 0.016).
    Conclusion: Integrating ISB and PIV provides improved prognostic stratification in patients with LARC treated with nCRT, identifying a high-risk subgroup with markedly inferior OS.
    Keywords:  Chemoradiotherapy; Immunoscore; Inflammation; Prognosis; Rectal Neoplasms; Tumor-Infiltrating Lymphocytes
    DOI:  https://doi.org/10.1016/j.ctro.2026.101172
  17. Front Immunol. 2026 ;17 1704419
      Chimeric antigen receptor (CAR) T cells represent an exciting therapeutic strategy with improved survival outcomes for patients with hematological malignancies. However, the efficacy of CAR T-cell therapy in the treatment of solid tumors remains suboptimal due to therapeutic barriers associated with the solid tumor microenvironment. We investigated whether ionizing radiation could improve vascular perfusion and CAR T-cell delivery in an EGFRvIII-expressing B16F10 melanoma model. Tumors received radiation doses of 2-12 Gy, and perfusion was evaluated at multiple time points using immunofluorescence detection of intravenously administered fluorescent dyes. We found that a single 8-Gy dose of ionizing radiation produced the most significant increase in B16F10 tumor perfusion 4 h after irradiation. Consistently, the irradiation of tumors 4 h prior to a systemic administration of EGFRvIII-targeting CAR T cells led to higher intratumoral CAR T-cell accumulation than in non-irradiated tumors. This approach also resulted in a significantly delayed tumor growth and improved survival relative to radiation or CAR T cells alone. Interestingly, the CD28ζ EGFRvIII-CAR T-cell levels substantially increased in irradiated tumors over time relative to 4-1BBζ EGFRvIII-CAR T cells and produced greater tumor growth delays and survival improvements in comparison to 4-1BBζ EGFRvIII-CAR T cells administered at a 10-fold higher concentration. Taken together, these data highlight the importance of co-stimulatory domains in CAR T-cell function in vivo and demonstrate that irradiating tumors prior to systemic CAR T-cell infusion can increase CAR T-cell infiltration and efficacy in solid tumors.
    Keywords:  CAR T cell therapy; ionizing radiation; melanoma; perfusion; solid tumors
    DOI:  https://doi.org/10.3389/fimmu.2026.1704419
  18. Immunity. 2026 Apr 29. pii: S1074-7613(26)00144-5. [Epub ahead of print]
      CD8+ T cells need to function in complex environments with varied nutrient availability, including the tumor microenvironment and inflamed tissues. The mechanisms that allow CD8+ T cells to maintain immune function in these perturbed settings are poorly understood. Here, we show that CD8+ T cells adapt to nutrient stresses over time, reconfiguring gene-regulatory and metabolic networks to license functional recovery. Under acute stress, T cells reoriented translational programming, which limited nutrient demand and prioritized stress-sensitive metabolic and transcriptional responses. Within these responses, the transcription factors activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein gamma (CEBPG) jointly established an adaptive metabolic program, promoting amino acid synthesis and uptake while maintaining mitochondrial metabolism. Despite diminished energetic capacity under environmental stress, this program sustained central carbon metabolism. This subsequently mitigated cellular dysfunction and potentiated anti-tumor immunity. Altogether, we demonstrate that biosynthetic plasticity via translational and metabolic reprioritization confers T cell resilience in unfavorable environments, offering potential strategies to enhance immunotherapies.
    Keywords:  ATF4; CD8(+) T cells; CEBPG; GCN2; HRI; T cell exhaustion; T cells; amino acids; anti-tumor immunity; immunometabolism; integrated stress response; mTOR; nutrient stress; polysome profiling; stress adaptation; translation; tumor-infiltrating lymphocyte
    DOI:  https://doi.org/10.1016/j.immuni.2026.04.004
  19. bioRxiv. 2026 Apr 15. pii: 2026.04.13.717612. [Epub ahead of print]
      Chimeric antigen receptor (CAR)-modified Vδ2 T cells are an attractive therapeutic cell platform for cancer immunotherapy. However, their clinical efficacy is limited by short in vivo persistence due to insufficient cytokine support and high susceptibility to activation-induced cell death (AICD). Through comparison of membrane-bound (mb) cytokines, we identified mbIL-18 to support superior anti-tumor activity of CAR-Vδ2 T cells in vitro and in vivo . To reduce constitutive surface exposure of IL-18 and enable antigen-driven signal 3, we fused MyD88 - the key IL-18R signaling mediator - to an extracellular domain of Fas (Fas88). Antigen stimulation-induced FasL engagement of Fas88 triggered IL-18 signaling while simultaneously protecting Vδ2 T cells from AICD. Fas88-armed human CAR-Vδ2 T cells produced superior yet stimulation-dependent in vivo expansion and functional persistence in xenograft models of hematologic and solid malignancies. Together, these findings highlight the importance of IL-18 signaling and AICD resistance for CAR-Vδ2 T cell activity, enabling a single-transgene modification to limit inflammatory risk and facilitate clinical translation.
    DOI:  https://doi.org/10.64898/2026.04.13.717612
  20. J Clin Invest. 2026 May 01. pii: e200987. [Epub ahead of print]136(9):
      Conventional type-1 dendritic cells (cDC1) are the main mediators of crosspresentation of tumor antigens to CD8+ T cells and provide a context of costimulatory molecules and cytokines that lead to cytotoxic T lymphocyte (CTL) responses. We analyzed bulk RNA sequences from 7 key clinical trials testing checkpoint inhibitors across multiple cancer types. cDC1- and CD8-associated gene signatures were analyzed. Multiplex tissue immunofluorescence was used to quantify cDC1 in melanoma, urothelial cancer, and non-small-cell lung cancer (NSCLC) samples and assess cDC1 tissue neighborhoods. Melanoma samples were studied with Xenium spatial transcriptomics (ST) and one series of NSCLC was analyzed using GeoMX-DSP. Strong associations across tumor types were found between cDC1 and CD8+ T cell transcripts with clinical outcomes. As mechanistically expected, transcripts for the CCL4 and CCL5 chemokines and the growth factor FLT3-L showed associations with cDC1 abundance. Tissue immunofluorescence showed a strong correlation of cDC1 and CD8+ T cell infiltration with clinical benefit upon treatment with checkpoint inhibitors (CPIs). Moreover, short distance between cDC1 and CD8+ T cells was found to define tissue niches associated with favorable outcomes. ST revealed recent T cell activation within immune cDC1-rich niches. cDC1 abundance, which determines CD8+ T lymphocyte density and activation in tumor tissues across cancer types, is strongly associated with clinical response to CPI-based immunotherapies.
    Keywords:  Cancer immunotherapy; Dendritic cells; Immunology; Oncology
    DOI:  https://doi.org/10.1172/JCI200987
  21. Mol Cancer Ther. 2026 Apr 29.
      Osteosarcoma (OS), the most common primary bone malignancy in adolescents and young adults, is still marked by poor long-term survival and poor mortality. Although immune checkpoint blockade (ICB) has transformed treatment for several cancers, its benefit in OS has been minimal, largely due to OS's "immune-cold" phenotype characterized by scarce tumor-infiltrating lymphocytes. Novel strategies are urgently needed to overcome this resistance. Y-box binding protein 1 (YB-1), a pro-oncogenic member of the cold-shock protein superfamily, represents a promising target to sensitize OS to ICB. Here, we evaluate SU056, a small-molecule YB-1 inhibitor, which both suppressed intrinsic OS tumor growth and remodeled the tumor microenvironment (TME). SU056 treatment markedly reduced immunosuppressive populations, including regulatory T cells (Tregs) and M2-polarized tumor-associated macrophages (TAMs), while enhancing infiltration of granzyme B-positive cytotoxic CD8⁺ T cell and NK cells. Combination therapy with SU056 and anti-PD-1 blockade produced superior tumor growth inhibition and significantly prolonged survival compared with either monotherapy. These findings highlight SU056 as a potent immunomodulatory agent and support its coadministration with ICB as a promising therapeutic approach for OS.
    DOI:  https://doi.org/10.1158/1535-7163.MCT-25-1240
  22. Br J Cancer. 2026 Apr 27.
      Adoptive cell therapies (ACT) and immune cell engagers (ICE) redirect or potentiate immune effector function against immune-tolerated antigens expressed on malignant cells, representing a distinct class of engineered immunotherapies beyond immune checkpoint blockade. These strategies have been particularly successful in hematologic malignancies; however, translation to solid tumours has been constrained by antigen heterogeneity, limited immune cell trafficking and persistence, an immunosuppressive tumour microenvironment, and on-target off-tumour toxicity. Despite these barriers, accumulating data and clinical experience with these therapies in solid tumours demonstrate feasibility, scalability, safety, and meaningful clinical activity. In light of recent regulatory approvals of ACT and ICE in solid tumours, we aim to provide a comprehensive clinician-oriented overview of these evolving therapeutic platforms. Herein, we review principles of antigen selection, mechanisms underlying investigational ACT and ICE, current barriers to clinical translation in solid tumours, strategies to overcome these limitations, and future prospects for immune-redirecting drug development in solid tumours.
    DOI:  https://doi.org/10.1038/s41416-026-03450-w
  23. Oncol Res. 2026 ;34(5): 10
      In vivo Chimeric Antigen Receptor (CAR)-T cell therapy reprograms a patient's own T cells directly inside the body, bypassing the complex and costly traditional manufacturing process. This is achieved by systemically delivering viral or non-viral vectors that genetically modify endogenous T lymphocytes to produce functional CAR-T cells de novo. By eliminating ex vivo cell processing, this strategy can simplify workflows, reduce costs, improve accessibility, and allow faster treatment. Key delivery platforms include engineered lentiviral and adeno-associated viral (AAV) vectors for lasting CAR expression and targeted lipid nanoparticles (LNPs) for transient mRNA delivery. Emerging technologies like biomaterial scaffolds and ultrasound stimulation further enable localized and spatiotemporally controlled T cell engineering. Clinically, early trials in relapsed/refractory multiple myeloma and B-cell malignancies have shown strong antitumor responses, even without preconditioning chemotherapy. Remaining challenges comprise achieving precise T cell targeting, overcoming the immunosuppressive tumor microenvironment, preventing antigen escape, and managing safety risks such as vector genotoxicity or LNP reactogenicity. Future translation will depend on combining synergistic regimens, refining vector design, and implementing tunable safety controls. The aim of the study is to highlight how in vivo CAR-T therapy is evolving from concept to clinical reality, poised to redefine adoptive cell therapy as a scalable and widely applicable pharmacologic intervention.
    Keywords:  Chimeric antigen receptor-T; cancer treatment; cell therapy; gene therapy; in vivo chimeric antigen receptor-T
    DOI:  https://doi.org/10.32604/or.2026.076420
  24. Semin Oncol. 2026 Apr 06. pii: S0093-7754(26)00042-4. [Epub ahead of print]53(3): 152495
       BACKGROUND: We have demonstrated that CXCL8⁺ monocyte-derived tumor-associated macrophages (TAMs) promote autonomous PD-L1 expression, thereby fostering an immunosuppressive tumor microenvironment. Nevertheless, the functional contribution of tissue-resident macrophages to immune escape remains largely unexplored.
    METHODS: The study incorporated four independent cohorts, including two tumor microarray datasets and two groups of transcriptomic profiling data. Associations between TREM2⁺TAMs and clinical outcomes as well as genomic features were evaluated. Additionally, ex vivo culture of fresh tumor tissues was conducted to evaluate the potential therapeutic efficacy of dual blockade targeting PD-1 and TREM2 in gastric cancer.
    RESULTS: TREM2⁺TAMs level was significantly associated with reduced overall survival in patients with resectable gastric cancer. Notably, a high density of TREM2⁺TAMs correlated with poorer response to immune checkpoint inhibitor. Mechanistically, TREM2⁺TAMs were found to drive CD8⁺T cell exhaustion through dual expression of PD-L1 and Arg1. Blockade of TREM2 sensitized tumors to pembrolizumab and enhanced antitumor immunity, particularly in tumors with high TREM2⁺TAMs infiltration.
    CONCLUSIONS: TREM2⁺TAMs infiltration served as an independent prognosticator in patients with gastric cancer. TREM2⁺TAMs promoted tumor immune escape through concomitant expression of PD-L1 and Arg1. Dual blockade targeting both PD-1 and TREM2 enhanced antitumor responses in TREM2⁺TAMshigh tumors, suggesting a promising therapeutic strategy for gastric cancer.
    Keywords:  Gastric cancer; Immune suppression; Macrophages; TREM2
    DOI:  https://doi.org/10.1016/j.seminoncol.2026.152495
  25. Front Immunol. 2026 ;17 1791059
      Interleukin-15 (IL-15) has emerged as a central cytokine for next-generation cancer immunotherapy because of its unique ability to sustain the survival, proliferation, and cytotoxic function of memory CD8+ T cells and natural killer (NK) cells without promoting the expansion of regulatory T cells (Treg). These properties make IL-15 particularly attractive for achieving durable antitumor immunity, especially in solid tumors where immune persistence remains a major limitation. Although IL-15 shares the same signal-transducing receptor subunits (IL-2Rβ and the common γ chain) with interleukin-2 (IL-2), the two cytokines drive fundamentally different CD8+ T-cell fates, a distinction that underlies their markedly divergent therapeutic profiles in cancer immunotherapy. In recent years, multiple IL-15-based therapeutic strategies including recombinant IL-15, and IL-15 immunocytokines have entered clinical evaluation, demonstrating potent immune activation with manageable toxicity profiles. Recent clinical progress includes the FDA approval of Nogapendekin alfa inbakicept (N-803), the first IL-15-based immunotherapy approved for cancer treatment, alongside the advancement of other IL-15 superagonists into Phase II trials and growing evidence that IL-15 can enhance the efficacy of immune checkpoint blockade and engineered adoptive cell therapies such as CAR-T cells, CAR-NK cells, γδ T cells, and invariant NKT cells. Despite these advances, important challenges remain, including cytokine-associated toxicities, optimal delivery strategies, and the immunosuppressive tumor microenvironment. This review summarizes recent progress in IL-15-based cancer immunotherapy, integrates emerging insights into IL-2Rβγ-driven CD8+ T-cell fate decisions, and discusses key opportunities and challenges for translating IL-15-mediated immune enhancement into durable clinical benefit.
    Keywords:  CAR-NK cells; CAR-T cells; cancer immunotherapy; cytokine engineering; immune checkpoint inhibitor (ICI); immunocytokines; interleukin-15 (IL-15); interleukin-2 (IL-2)
    DOI:  https://doi.org/10.3389/fimmu.2026.1791059
  26. Nature. 2026 Apr 29.
      Although intrinsic metabolic pathways have critical roles in T cell function1,2, systemic nutrient availability is in constant flux. Yet, how postprandial metabolism affects T cell fate has been less studied. Here we show that the short-term nutritional state of an individual has marked effects on T cell immunity. Human or murine T cells from fed hosts had higher metabolic capacity than those from fasted hosts, and this increase in capacity persisted after activation and expansion in vitro or in vivo. Triglyceride-rich chylomicrons in serum were drivers of postprandial immunometabolic reprogramming, and chylomicrons primed mTORC1-dependent translation ex vivo and after activation, which markedly enhanced effector function after priming. Human postprandial CAR-T cells manufactured from the same donor showed a therapeutic advantage over T cells collected while individuals were fasted. Thus, postprandial metabolism imparts durable metabolic and functional advantages to T cells, highlighting the importance of considering nutritional status in immunological analysis, vaccination and generation of cellular therapies.
    DOI:  https://doi.org/10.1038/s41586-026-10432-8
  27. Biomaterials. 2026 Apr 27. pii: S0142-9612(26)00274-7. [Epub ahead of print]334 124250
      The immunosuppressive tumor microenvironment (TME) of B-cell lymphoma limits the efficacy of conventional chemotherapy and hampers the full activation of antitumor immunity. Here, we report a tumor cell membrane-camouflaged nanoplatform (CM@HFeS/DOX/MSA-2) that couples ferroptosis amplification with cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway activation to overcome these barriers. The HFeS nanozyme promotes lipid peroxidation (LPO) and reactive oxygen species (ROS) generation, while doxorubicin (DOX) augments immunogenic cell death (ICD) and facilitates cytosolic DNA accumulation, thereby potentiating MSA-2-mediated STING activation. In vitro and in vivo, CM@HFeS/DOX/MSA-2 synergistically induces ferroptosis, enhances ICD hallmarks, and drives robust dendritic cell (DC) maturation. In an A20 B-cell lymphoma model, this biomimetic nanoplatform markedly suppresses tumor growth, increases intratumoral CD8+ T-cell and DC infiltration, and reduces immunosuppressive macrophages. Imaging mass cytometry and transcriptomic profiling further identify granzyme B (GzmB)+CD38+CD8+T cells and major histocompatibility complex class II (MHCII)+CD103+ CD4+T cells as key effector populations within the remodeled TME. Immune cell depletion experiments support a critical role for CD8+ T cells and the DC-associated immune axis in mediating therapeutic efficacy. Moreover, CM@HFeS/DOX/MSA-2 sensitizes tumors to anti-programmed cell death protein 1 (PD-1) checkpoint blockade and confers strong vaccine-like protection in tumor rechallenge models. Together, this study presents a rationally engineered nanoplatform that coordinately activates ferroptosis and cGAS-STING signaling to reprogram the lymphoma immune landscape and achieve robust, durable antitumor immunity.
    Keywords:  Biomimetic nanoplatform; Ferroptosis; ICD; Lymphoma; Tumor microenvironment modulation; cGAS-STING
    DOI:  https://doi.org/10.1016/j.biomaterials.2026.124250