bims-tuinly Biomed News
on Tumor-infiltrating lymphocytes therapy
Issue of 2026–08–09
sixteen papers selected by
Pierpaolo Ginefra, Ludwig Institute for Cancer Research



  1. Endocr Relat Cancer. 2026 Aug 05. pii: ERC-25-0411. [Epub ahead of print]
       BACKGROUND: This study investigated the associations between tumor-infiltrating lymphocytes (TILs), genomic features, and prognosis in HER2+ early breast cancer (EBC) patients receiving adjuvant trastuzumab.
    MATERIALS AND METHODS: We retrospectively analyzed 864 HER2+ EBC patients from Shanghai Ruijin Hospital (2009-2017). The optimal threshold of TILs for predicting disease free survival (DFS) and overall survival (OS) was explored. Whole-exome sequencing (WES) on 261 tumors assessed the mutational profiles, tumor mutational burden (TMB), and copy number alteration (CNA). Associations of these genomic features, TILs levels and prognosis were further evaluated.
    RESULTS: TILs showed a right-skewed distribution (median 15%, IQR 1-30%), and higher TILs were significantly associated with hormone receptor negativity and high histologic grade (p < 0.001). A 15% TILs threshold optimally predicted prognosis, with low TILs (≤15%, 63.0%) patients showing inferior DFS (HR 1.63, p = 0.009) and OS (HR 2.12, p = 0.037). WES identified frequent mutations in TP53 (62.8%), PIK3CA (34.5%), and BRCA2 (9.6%). Higher TILs density was observed in TP53-wild-type, low-TMB or low-CNA tumors (p < 0.05). PIK3CA mutations conferred a significant DFS advantage. Integrating TILs level with PIK3CA or BRCA2 mutational status yielded distinct DFS trajectories (log-rank p = 0.023 and 0.040, respectively); patients with both high TILs and either PIK3CA or BRCA2 mutations had the most favorable outcomes.
    DISCUSSION: Stromal TILs at a 15% cut-off provide robust prognostic information in trastuzumab-treated HER2+ EBC. Integrating TILs levels with PIK3CA or BRCA2 mutational status enables refined risk stratification, offering a practical framework for personalized treatment decisions.
    Keywords:  Breast Neoplasms; Exome Sequencing; Prognostic Factors; Retrospective Studies; Trastuzumab; Tumor-infiltrating Lymphocytes
    DOI:  https://doi.org/10.1530/ERC-25-0411
  2. Front Oncol. 2026 ;16 1859306
       Purpose: Adoptive tumor-infiltrating lymphocyte (TIL) therapy is an established personalized cellular immunotherapy with demonstrated activity in selected solid tumors, particularly metastatic melanoma. However, clinical outcomes, safety, and manufacturing feasibility vary across tumor types and treatment strategies. This systematic review evaluates the efficacy, safety, and operational characteristics of TIL therapy across solid malignancies.
    Methods: This systematic review was conducted in accordance with PRISMA guidelines. PubMed, Scopus, the Cochrane Central Register of Controlled Trials, and the WHO International Clinical Trials Registry Platform were searched from inception to 31 December 2025. Eligible studies included clinical trials and observational studies evaluating autologous TIL therapy in solid tumors. Due to substantial clinical and methodological heterogeneity, quantitative synthesis was restricted to clinically comparable cohorts, predominantly melanoma studies reporting objective response rates (ORR). A single-arm random-effects meta-analysis using the Freeman-Tukey transformation was performed. All other outcomes, including survival, safety, manufacturing success, and resection-to-infusion time, were synthesized narratively.
    Results: Thirty-eight studies were included: 5 randomized controlled trials (RCTs), 22 prospective non-randomized studies, and 11 retrospective analyses, spanning melanoma and 8 other solid tumour types. Meta-analysis of 18 melanoma single-arm cohorts demonstrated a pooled objective response rate (ORR) of 42% (95% CI 37%-47%; I² = 33.1%; prediction interval 29%-56%) under a random-effects model. In the phase III RCT (Rohaan et al.), TIL therapy produced superior ORR (49% vs. 21%) and progression-free survival (median 7.2 vs. 3.1 months; HR 0.50, 95% CI 0.35-0.72) compared with ipilimumab. Subgroup analysis by TIL product type revealed a statistically significant difference (χ² = 7.25, p = 0.0266): tumor-reactive TIL products pre-screened ex vivo for antigen-specific reactivity showed the highest pooled ORR at 50% (95% CI 35%-64%), followed by young TIL at 43% (95% CI 29%-58%) and bulk TIL at 36% (95% CI 31%-42%); this observation is based on only 4 cohorts with a limited aggregate patient number and should be regarded as hypothesis-generating. No significant difference in ORR was observed by lymphodepletion status (p = 0.9544). Evidence in non-melanoma solid tumours was limited and heterogeneous, with generally lower response rates. Safety profiles were consistent across studies and primarily attributable to lymphodepleting chemotherapy and interleukin-2 administration, including haematologic and cytokine-related toxicities; treatment-related mortality was uncommon. Manufacturing success rates were high across contemporary cohorts, with a resection-to-infusion time typically spanning 4-6 weeks.
    Conclusion: TIL therapy demonstrates consistent and clinically meaningful antitumor activity in melanoma, while evidence in non-melanoma tumors remains limited and heterogeneous. Future studies should prioritize biomarker-driven patient selection, optimization of manufacturing and conditioning strategies, and rational combination approaches to expand its applicability.
    Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420261291389.
    Keywords:  adoptive cell therapy; meta-analysis; solid tumors; systematic review; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.3389/fonc.2026.1859306
  3. Proc Natl Acad Sci U S A. 2026 Aug 11. 123(32): e2517883123
      Adoptive cell transfer of tumor infiltrating CD4+ T cells or T cells genetically modified to express antitumor CD4+ T cell receptors (TCRs) has shown clinical efficacy in patients with advanced solid tumors. We previously defined unique transcriptomic states of antitumor, neoantigen-specific CD8+ and CD4+ tumor infiltrating lymphocytes (TIL) in human cancer. However, optimal cell surface protein markers that identify and would enable viable cell isolation and selective enrichment of antitumor CD4+ T cells have yet to be identified. Here, we define transcriptomic and corresponding cell surface protein profiles of antitumor CD4+ TIL within metastatic colorectal tumors using high dimensional single cell transcriptomic and proteomic analysis. Comprehensive analysis of 45 antitumor CD4+ TCR clonotypes demonstrated uniquely high cell surface protein expression of ADGRG1, CD86, and CD57. In all samples containing tumor neoantigen-reactive CD4+ TIL clonotypes, ADGRG1- and CD86-based cell surface enrichment of known reactive TCR clonotypes were 11-fold and 9-fold higher than bulk CD4+ TIL, respectively. ADGRG1- and CD86-based cell surface enrichment identified >60 validated antitumor CD4+ TCR-clonotypes including tumor organoid-reactive TCRs, as well as neoantigen-specific TCRs targeting private tumor mutations and cancer driver mutations. While both ADGRG1 and CD86 enriched CD4+ TIL displayed an exhausted neoantigen-specific gene expression signature, CD86 also enriched for cytotoxic CD4+ TIL phenotypes. CD4+ TIL isolated based on ADGRG1 expression and expanded in vitro also demonstrated neoantigen reactivity in two samples. Thus, ADGRG1 and CD86 appear to be effective protein markers for isolating human tumor-specific CD4+ TCR clonotypes and studying antitumor CD4+ TIL.
    Keywords:  ADGRG1; CD4; T cell; cancer; neoantigen
    DOI:  https://doi.org/10.1073/pnas.2517883123
  4. Front Immunol. 2026 ;17 1844781
       Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies to date and characterized by a unique immunosuppressive and highly desmoplastic tumor microenvironment (TME). These features drive profound T-cell dysfunction and maintain high resistance to current immunotherapy. By recapitulating the complex 3D architecture of human PDAC, we demonstrate the key immunosuppressive mechanisms that drive T-cell dysfunction within the tumor microenvironment.
    Method: 3D PDAC spheroids-generated from PANC-1 cells alone or together with primary pancreatic stellate cells (PSC)-were infiltrated with primary human T-cells from healthy donors, allowing controlled analysis of T-cell infiltration, activation, and checkpoint regulation. Furthermore, patient-derived spheroids (PDS) composed of primary tumor cells and cancer-associated fibroblasts were infiltrated with autologous T-cells.
    Results: Infiltrated T-cells exhibited a pronounced exhaustion signature, including strong upregulation of PD-1, LAG-3, and CTLA-4, closely mirroring the phenotype of tumor-infiltrating lymphocytes (TIL) isolated from PDAC patient samples. Incorporation of pancreatic stellate cells (PSC) generated a fibrotic barrier around the tumor cells that markedly restricted T-cell infiltration, modeling the desmoplastic TME characteristic of PDAC. From a mechanistic perspective, stromal CXCL12-CXCR4 enhanced T-cell exclusion: pharmacological CXCR4 blockade with AMD3100 significantly enhanced T-cell infiltration into PSC-containing spheroids. Furthermore, treatment with the anti-PD-1 monoclonal antibody pembrolizumab partially restored the effector cell function of T-cells within the 3D system. These results demonstrate that this minimalistic platform is capable of capturing complex, cytokine- and stroma-driven immunomodulation typically observed only in advanced organoid or in vivo systems. Crucially, key immunological features-including T-cell exhaustion, stromal exclusion, and therapeutic responsiveness-were fully reproduced in PDS. PDS reproduced patient-specific T-cell suppression patterns and therapeutic responses, underscoring the translational relevance of the platform.
    Conclusion: Together, our findings identify critical determinants of T-cell dysfunction in PDAC and introduce a versatile, animal-free 3D model that powerfully captures hallmark immune-evasion mechanisms in PDAC. This system provides a scalable and mechanistically faithful tool for dissecting TME-driven immune suppression and for accelerating the functional evaluation of immunotherapeutic strategies, including patient-tailored approaches.
    Keywords:  CXCR4; PD-1; T-cell exclusion; T-cell exhaustion; immune checkpoints; pancreatic ductal adenocarcinoma; patient-derived spheroids; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2026.1844781
  5. BMB Rep. 2026 Aug 03. pii: 6874. [Epub ahead of print]
      T cell-based immunotherapies have transformed the treatment of hematological malignancies, but their efficacy in solid tumors remains inconsistent. Unlike blood cancers, solid tumors present multiple barriers that impede T cell infiltration, metabolic fitness, antigen recognition, and long-term persistence. These barriers include structural exclusion by the stroma, tumor-driven metabolic competition, antigen plasticity, and the progressive epigenetic fixation of T cell exhaustion states. This review integrates our current understanding of T celldirected therapeutic approaches and examines the tumorintrinsic and microenvironmental mechanisms that limit their activity in solid malignancies. We discuss how chronic stress signaling, altered nutrient availability, glycan-mediated epitope masking, and transcriptional reprogramming collectively destabilize therapeutic T cell function. Finally, we evaluate emerging strategies designed to remodel the tumor niche, diversify antigen targeting, and enhance T cell metabolic and epigenetic resilience. Thus, developing a mechanistic framework that combines intrinsic T cell reprogramming with adaptation to the tumor context will be crucial for extending durable T cell-mediated immunity to solid cancers.
  6. Front Immunol. 2026 ;17 1933173
      [This corrects the article DOI: 10.3389/fimmu.2026.1755657.].
    Keywords:  CD8+ T cells; CX3CR1 subset differentiation; NOSIP; PD-L1 blockade responsiveness; chronic antigen stimulation
    DOI:  https://doi.org/10.3389/fimmu.2026.1933173
  7. Biochem Biophys Res Commun. 2026 Aug 06. pii: S0006-291X(26)01149-6. [Epub ahead of print]832 154385
      Immune checkpoint blockade elicits durable responses in a subset of patients with gastric cancer, yet the cellular programs underlying therapeutic divergence remain unclear. Using integrative single-cell transcriptomics of tumors from Immune Checkpoint Inhibitor (ICI)-treated patients, we resolved the CD8 + T-cell landscape associated with response. Therapeutic outcome reflected not only differences in state abundance but also functional reprogramming within shared states. Trajectory analysis revealed bifurcation of naïve CD8 + T cells into effector and exhaustion-prone branches that were differentially enriched between responders and non-responders. Inference of transcription factor activity revealed lineage-specific modules associated with these divergent fates. Further modeling of ligand-receptor pairs uncovered how signaling between myeloid and T cells changes during different responses. Together, these findings delineate a regulatory and intercellular framework characterizing CD8 + T-cell differentiation in gastric cancer and illuminate mechanisms of immune-state divergence during immunotherapy.
    Keywords:  Gastric cancer; Immune checkpoint inhibitor; scRNA-seq
    DOI:  https://doi.org/10.1016/j.bbrc.2026.154385
  8. Crit Rev Oncol Hematol. 2026 Aug 06. pii: S1040-8428(26)00404-X. [Epub ahead of print] 105517
      Small cell lung cancer (SCLC) is an aggressive malignancy with limited treatment options, and the integration of immune checkpoint inhibitors (ICIs) into treatment regimens has reshaped the therapeutic landscape. However, challenges such as rapid resistance and lack of effective predictive biomarkers remain. This review highlights the pivotal roles of biomarkers in SCLC, underscoring their contributions to treatment resistance across tumor-intrinsic mechanisms, immune landscape of the tumor microenvironment (TME) and systemic host factors. Tumor-intrinsic features, including molecular subtypes, genetic alterations such as TP53 and RB1 mutations, and tumor mutation burden (TMB), have shown varying associations with ICI efficacy. Notably, the SCLC-I (inflamed) molecular subtype appears more responsive to immunotherapy. Within the TME, programmed cell death ligand 1 expression, tumor-infiltrating lymphocytes (TILs), regulatory T cells, myeloid-derived suppressor cells, and tissue-associated cytokines and chemokines contribute to immune modulation. High CD8+ TILs are linked to better outcomes, while increased immunosuppressive populations often suppress anti-tumor response. Systemic factors, encompassing both tumor-derived (ctDNA, CTCs, tumor-derived EVs) and host-derived (circulating immune cell phenotypes, MHC expression, immune profile, baseline clinical characteristics) components, provide valuable insights into treatment response and prognosis. Further research is needed to validate biomarkers and investigate combination approaches to overcome resistance, offering hope for improved patient outcomes in SCLC.
    Keywords:  Biomarker; Immune checkpoint inhibitor; Immunotherapy; Small cell lung cancer
    DOI:  https://doi.org/10.1016/j.critrevonc.2026.105517
  9. Breast Cancer. 2026 Aug 03.
       BACKGROUND: Pentraxin 3 (PTX3) is an inflammatory mediator involved in tumorigenesis; however, its role in tumor immune evasion remains elusive. Herein, we demonstrate that PTX3 promotes immune evasion in breast cancer by upregulating PD-L1.
    METHODS: RT-qPCR and Western blot were performed to assess PD-L1 expression in human and murine breast cancer cells. Cell surface PD-L1 was assayed by flow cytometry. Small interfering RNA and CRISPR-Cas9 were used to inhibit PTX3 expression. Co-culture experiments were conducted to evaluate the suppressive effects of tumor cells on CD8 + T cell activation. An immunocompetent BALB/c mouse allograft model was utilized, and tumor-infiltrating CD8 + T cells were analyzed by flow cytometry and immunohistochemistry.
    RESULTS: PTX3 enhanced PD-L1 protein levels through the inhibition of autophagy. PTX3 increased the expression of the E3 ligase RNF216 and caused Beclin-1 degradation, which suppressed autophagy, thereby preventing autophagy-mediated PD-L1 degradation. Co-culture experiments demonstrate that PTX3-overexpressing breast cancer cells suppressed CD8 + T cell function, as evidenced by reduced production of IFN-γ and Granzyme B, whereas PTX3-depleted cells had the opposite effects. In vivo allograft studies revealed that depletion of PTX3 reduced PD-L1 expression, enhanced CD8 + T cell infiltration, and inhibited tumor growth in immunocompetent mice.
    CONCLUSION: PTX3 promotes PD-L1 expression and immune evasion in breast cancer. Therefore, targeting PTX3 may represent a potential therapeutic strategy to counteract this immune escape.
    Keywords:  CRISPR-Cas9; Genetic diagnosis; Long-read sequencing; Neurogenetics; Nucleotide repeats
    DOI:  https://doi.org/10.1007/s12282-026-01902-y
  10. Sci Adv. 2026 Aug 07. 12(32): eadp2955
      Adoptive T cell therapy requires T cells to infiltrate vascular tissues and preserve immune function. In solid tumor treatment, however, the surrounding microenvironment produces abnormal vasculature that impedes T cell infiltration. An approach that enables vascular normalization and enhances adoptive T cell function in parallel is essential for effective therapy but has not been reported. Here, we report the use of lenvatinib (LEN) to induce transient vascular normalization, thereby facilitating T cell infiltration. Moreover, LEN enhances T cell persistence by promoting the differentiation of T cells toward a memory phenotype. Our results indicate that the differentiation is by suppressing the PI3K-AKT-mTOR pathway, which drives effector differentiation, and by activating FOXO1, a transcription factor that promotes memory formation. To coordinate the transient vascular normalization and T cell enhancement, we link LEN-loaded, PD-L1-blocking micelles to T cells through acid-labile click chemistry, forming pH-responsive T cell-nanodrug conjugates. The conjugates synchronize the intratumoral release of LEN and the PD-L1 antagonist peptide OPBP-1, thereby coordinating vascular normalization, T cell differentiation, and checkpoint blockade. In vivo, the conjugates increased intratumoral CD8+ T cells and splenic memory T cells by over sixfold in B16-OVA tumors and achieved complete regression in a subset of MC38-OVA tumors without systemic toxicity, providing a promising strategy for solid tumor immunotherapy.
    DOI:  https://doi.org/10.1126/sciadv.adp2955
  11. Front Immunol. 2026 ;17 1880908
      Glioblastoma (GB) remains one of the most aggressive brain tumours, with a median survival of 15 months, largely due to resistance towards available anti-cancer therapies, including cutting-edge immunotherapy. Growing evidence indicates involvement of cancer stem cells (CSCs) in escalating resistance against existing treatment modalities due to their phenotypic plasticity, elevated expression of drug-resistance pumps, and immunomodulatory behaviour. Such oncogenic consequences are regulated by several epigenetic reprogramming events that are pivotal in retaining adaptive traits associated with CSC-mediated therapy resistance and subsequent oncogenic progression. In this review, we consider such epigenetic consequences as "tumour memory" and try to shed light on the therapeutic vulnerabilities by targeting CSCs - the "carriers of tumour memory" - via immune interventions in GB. Interestingly, immune-based anti-cancer therapies are coming to the forefront of cancer research, where T lymphocytes are immunologically boosted to attack tumour cells. However, in reality, several constraints burden such procedures. Contextually, the GB microenvironment, dominated by bone marrow-derived cells, reprograms infiltrating immune cells into suppressor phenotypes, creating a "cold" immune landscape. The only zone where functionally active lymphocytes are preserved is the invasive margin of the tumour, where they undergo exhaustion along the TPE → TEX axis but retain proliferative potential. On this basis, we introduce the concept of "invasive margin lymphocytes" (IMLs), of which stem-like memory T cells (TSCM) are indispensable for long-term immunological protection, as they have unique proliferative potential and ability for long-term persistence. Incidentally, such TSCMs have striking similarities with CSCs, as both cell types employ evolutionarily conserved mechanisms of the WNT/β-catenin signalling pathway, hierarchical organisation, and DNA repair systems. Therefore, understanding CSC-TSCM bidirectional cross-talk could provide a heuristic basis for developing personalised TIL-based therapy aimed at suppressing the hierarchically organised CSC population and overcoming CSC-guided immunotherapy resistance. Drawing conceptual parallels between GB CSCs and TSCM, here in this review, we propose a three-stage therapeutic strategy: precision cytoreduction of the invasive margin, "warming up" the microenvironment using cancer vaccines and pharmacological agents, as well as adoptive transfer of TILs derived from the IML pool to ensure durable disease control.
    Keywords:  T memory stem cells (TSCM); cancer stem cells; glioblastoma; microenvironment; tumour-infiltrating lymphocytes (TILs)
    DOI:  https://doi.org/10.3389/fimmu.2026.1880908
  12. J Immunol. 2026 Aug 04. pii: vkag166. [Epub ahead of print]215(8):
      Cancer patient-derived T cells often exhibit impaired activation and functional responsiveness due to chronic antigen exposure and therapy-induced immune dysregulation, limiting the efficacy of current immunotherapies. Mechanical forces, such as fluid shear stress (FSS), are emerging as critical regulators of immune cell activation, yet their role in modulating activation of patient-derived T cells remains largely unexplored. In this study, primary T cells isolated from patients with metastatic prostate cancer were exposed to FSS using a cone-and-plate viscometer during ex vivo activation in the presence and absence of bead-bound anti-CD3/CD28 monoclonal antibodies. FSS alone was sufficient to induce NF-κB phosphorylation and intracellular cytokine synthesis, demonstrating that mechanical stimulation can independently initiate T cell activation signaling. Moreover, FSS combined with anti-CD3/CD28 stimulation produced a synergistic increase in activation signaling, IL-2 and IFN-γ production, and CD25/CD69 expression. While trends were consistent across donors overall, inter-patient variability reflected differences in baseline T cell phenotype, with naïve-like cells displaying greater mechanosensitivity. These results indicate that cancer patient-derived T cells retain mechanotransduction capacity despite reduced antigen responsiveness. Incorporating FSS as a co-stimulatory signal during ex vivo expansion may be more effective at priming patient T cells for activation, enhancing effector function, and improving the efficacy of adoptive cell therapies.
    Keywords:  T cell activation; immunotherapy; mechanobiology; prostate cancer
    DOI:  https://doi.org/10.1093/jimmun/vkag166
  13. Adv Drug Deliv Rev. 2026 Aug 03. pii: S0169-409X(26)00174-2. [Epub ahead of print] 115940
      In vivo reprogramming of T cells represents a transformative approach in immune-based therapies, with the potential to overcome the limitations of traditional ex vivo-engineered T cell products, such as autologous CAR-T therapies. While CAR-T cells have achieved remarkable success in treating hematological cancers with several FDA approved products, challenges like manufacturing complexity, costs, toxicity, and relapse rates persist. In this review, we first provide a brief background on T cell biology and CAR T cells, and then present a comprehensive overview of emerging strategies for direct in vivo T cell reprogramming. We discuss the key platform technologies, including lipid nanoparticles and viral vectors, and the targeting methods employed to enhance delivery and efficacy. Moreover, we evaluate the functional state of reprogrammed T cells and the role of different mouse models and reporter systems in assessing their therapeutic potential. We highlight key challenges related to the biodistribution, activation, and persistence of modified T cells, with an emphasis on the potential of these strategies for treating not only blood cancers but also solid tumors, autoimmune diseases, and beyond. Finally, we provide an outlook on future directions by highlighting recent non-human primate studies, ongoing clinical activities, and strategic acquisitions, representing key innovations and discuss remaining translational hurdles in the field.
    Keywords:  CAR-T cells; In vivo; LNPs; Non-viral vectors; RNA; T cell reprogramming; Viral vectors
    DOI:  https://doi.org/10.1016/j.addr.2026.115940
  14. J Leukoc Biol. 2026 Aug 03. pii: qiag106. [Epub ahead of print]
      Emerging evidence has highlighted the influence of cellular metabolism on both cancer and T cell growth and survival, including in the context of adoptive cell immunotherapy. It is known that T cells heavily rely on glycolysis for cell proliferation and mediating effector functions. However, less is known about the role of the pentose phosphate pathway (PPP), a parallel metabolic pathway that produces antioxidant and biosynthetic precursors, towards regulating antitumor T cell function. In this review, we summarize the PPP's role as a time-dependent regulator of T cell activation and redox balance, and its association with improved functional capacity in exhausted T cells. We further highlight the contrasting role of the PPP for CD8+ and CD4+ T cell differentiation in guiding antitumor responses, as well as a unique connection in the glycogen-PPP axis to CD8+ memory T cells. Finally, we summarize global metabolic regulators that drive expression of PPP enzymes and discuss future avenues for immunotherapy that could take advantage of our current understanding of the PPP's role in T cell metabolism.
    Keywords:  T cell activation; T cells; antioxidants; cancer immunotherapy; glycolysis; pentose phosphate pathway
    DOI:  https://doi.org/10.1093/jleuko/qiag106
  15. Front Immunol. 2026 ;17 1892919
       Background: High-risk human papillomavirus (HR-HPV) infection is the primary driver of cervical cancer. Emerging evidence indicates that the tumor microenvironment (TME) undergoes severe metabolic rewiring, which may accelerate T cell exhaustion (TEX) and impair immune checkpoint blockade (ICB). However, the molecular mechanisms coupling HPV-driven metabolism to T cell dysfunction remain incompletely elucidated.
    Methods: This review summarizes immunometabolic interactions in the cervical cancer TME. We examined the metabolic alterations induced by HPV oncoproteins (E6/E7) and how they reshape nutrient availability, lactate accumulation, and lipid peroxidation to drive anti-tumor CD8+ T cell exhaustion.
    Results: HPV-driven aerobic glycolysis and IDO1-mediated tryptophan catabolism establish severe metabolic barriers, causing nutrient deprivation and histone lactylation in infiltrating lymphocytes. These alterations are associated with persistent mitochondrial stress and ferroptosis, accelerating terminal TEX. In preclinical models, natural products (e.g., curcumin, berberine, quercetin, and artemisinin derivatives) can counteract this immunosuppressive rewiring by targeting checkpoints such as HIF-1α, PKM2, and AMPK; however, direct evidence of CD8+ tumor-infiltrating lymphocyte rescue in HPV-specific immune-competent systems remains limited, largely inferred from other tumor types. Nanomedicine delivery may further enhance the bioavailability and targeting of these herbal components.
    Conclusion: HPV-induced metabolic reprogramming is proposed to act as a fundamental checkpoint driving T cell exhaustion in cervical cancer. Targeting these immunometabolic barriers using natural compounds, particularly via nanomedicine-based delivery strategies, represents a promising but still largely preclinical avenue to synergize with conventional immunotherapies and potentially overcome resistance.
    Keywords:  T cell exhaustion; cervical cancer; human papillomavirus; metabolic reprogramming; natural products; tumor microenvironment
    DOI:  https://doi.org/10.3389/fimmu.2026.1892919