bims-tuinly Biomed News
on Tumor-infiltrating lymphocytes therapy
Issue of 2025–06–15
eleven papers selected by
Pierpaolo Ginefra, Ludwig Institute for Cancer Research
  1. Anti-TNFR2 antibody and HMGN1 combined with TIL cell therapy inhibits colorectal cancer progression by enhancing immune response.
  2. Targeting tumor metabolism to augment CD8+ T cell anti-tumor immunity.
  3. Roles and functions of tumor-infiltrating lymphocytes and tertiary lymphoid structures in gastric cancer progression.
  4. T lymphocyte heterogeneity in NSCLC: implications for biomarker development and therapeutic innovation.
  5. Adoptive Cell Transfer of Tumor-Infiltrating Lymphocytes for Metastatic Acral Lentiginous Melanoma.
  6. Targeting B and T lymphocyte attenuator in cancer immunotherapy.
  7. Enhanced anti-tumor activity by zinc finger repressor-driven epigenetic silencing of immune checkpoints and TGFBR2 in CAR-T cells and TILs.
  8. Immunohistochemical expression of PD1, LAG3, and CTLA4 in diffuse large B cell lymphoma, clinicopathological correlation, and prognostic value.
  9. Tumoral pSMAD2 as a prognostic biomarker in early-stage breast cancer: insights from the randomized SweBCG91RT trial.
  10. CTLA-4 blockade in ovarian cancer immunotherapy: Mechanisms and clinical strategies.
  11. Intratumoral IL-33 + CD4 + FoxP3 + regulatory T cell infiltration determines poor clinical outcomes and intensive immunoevasive contexture in patients with pancreatic cancer after surgical resection: a cohort study.
  1. Biochem Biophys Res Commun. 2025 Jun 02. pii: S0006-291X(25)00859-9. [Epub ahead of print]775 152145
    Anti-TNFR2 antibody and HMGN1 combined with TIL cell therapy inhibits colorectal cancer progression by enhancing immune response.
    Hang Lv, Yujie Nie, Huan Gui, Haohua Yuan, Qianyu Jing, Shuanghui Chen, Linzhao Li, Quan Wan, Liming Zhao, Shengwen Zhou, Shuyi Wang, Jia Song, Yingjie Nie.
       BACKGROUND: Immunotherapy utilizing tumor-infiltrating lymphocytes (TILs) has demonstrated exceptional effectiveness in the treatment of diverse solid tumors. However, existing procedures typically involve lymphodepleting chemotherapy using cyclophosphamide and high-dose IL-2 to support the proliferation and activity of reintroduced TILs, despite the common occurrence of systemic toxicity.
    METHODS: A CT26 colorectal cancer mouse model was established in this research. Tumor tissues were removed, and TILs were isolated and cultured in vitro. The TIL identity was validated via flow cytometry. Mice received treatment with an anti-TNFR2 antibody, HMGN1, and TILs to assess the effectiveness of this new immune-combination therapy against tumors. Flow cytometry was employed to analyze CD8+ T cells, CD4+ T cells, and Treg cells, with TIL function evaluated using CCK8 assays.
    RESULTS: Administration of anti-TNFR2 antibody and HMGN1 not only stimulated TIL proliferation but also suppressed Treg cells within tumor tissues, thereby markedly enhancing TIL-mediated anti-tumor activity in mice. Mice receiving this combination therapy achieved complete tumor eradication and significantly prolonged survival. This immune-combination therapy also demonstrated substantial tumor suppression in the 4T1 breast cancer mouse model.
    CONCLUSION: The combined treatment of the anti-TNFR2 antibody and HMGN1 therapy synergistically alleviates immunosuppression by decreasing tumor-infiltrating regulatory T cells (Treg cells). This decrease in Treg cells results in the successful eradication of tumors in vivo by promoting the function and expansion of TIL.
    Keywords:  Adoptive cell therapy; Colon cancer; HMGN1; Immunotherapy; TNFR2; Tumor-infiltrating lymphocyte
    DOI:  https://doi.org/10.1016/j.bbrc.2025.152145
  2. J Pharm Anal. 2025 May;15(5): 101150
    Targeting tumor metabolism to augment CD8+ T cell anti-tumor immunity.
    Huan Liu, Wenyong Yang, Jingwen Jiang.
      CD8+ T cell-based immune-therapeutics, including immune checkpoint inhibitors and adoptive cell therapies (tumor-infiltrating lymphocytes (TILs), T cell receptor-engineered T cells (TCR-T), chimeric antigen receptor T cells (CAR-T)), have achieved significant successes and prolonged patient survival to varying extents and even achieved cure in some cases. However, immunotherapy resistance and tumor insusceptibility frequently occur, leading to treatment failure. Recent evidences have highlighted the ponderance of tumor cells metabolic reprogramming in establishing an immunosuppressive milieu through the secretion of harmful metabolites, immune-inhibitory cytokines, and alteration of gene expression, which suppress the activity of immune cells, particularly CD8+ T cells to evade immune surveillance. Therefore, targeting tumor cell metabolic adaptations to reshape the immune microenvironment holds promise as an immunomodulatory strategy to facilitate immunotherapy. Here, we summarize recent advances in the crosstalk between immunotherapy and tumor reprogramming, focusing on the regulatory mechanisms underlying tumor cell glucose metabolism, amino acid metabolism, and lipid metabolism in influencing CD8+ T cells to provide promising metabolic targets or combinational strategies for immunotherapy.
    Keywords:  CD8+ T cell; Immunotherapy; Metabolism reprogramming; TME; Tumor
    DOI:  https://doi.org/10.1016/j.jpha.2024.101150
  3. Front Immunol. 2025 ;16 1595070
    Roles and functions of tumor-infiltrating lymphocytes and tertiary lymphoid structures in gastric cancer progression.
    Zhiyuan Yao, Gengchen Li, Di Pan, Zichen Pei, Yan Fang, Haonan Liu, Zhengxiang Han.
      Gastric cancer (GC), a leading cause of cancer mortality, exhibits profound molecular heterogeneity and immunosuppressive tumor microenvironment (TME) features that limit therapeutic efficacy. This review elucidates the dual roles of tertiary lymphoid structures (TLS) and tumor-infiltrating lymphocytes (TILs) in GC progression. TLS, ectopic lymphoid organs formed under chronic inflammation, correlate with improved survival and immunotherapy sensitivity by fostering effector T/B cell interactions and antigen presentation. Conversely, immunosuppressive TME components like regulatory T cells (Tregs) and tumor-associated macrophages (TAMs) drive immune evasion via cytokine-mediated suppression and checkpoint activation (PD-1/PD-L1). CD8+ T cells exert context-dependent effects, with high infiltration reducing recurrence risk but paradoxically inducing exhaustion in PD-L1-rich microenvironments. Th17 and memory T cells further modulate disease through IL-17-driven angiogenesis and CD45RO+ immune memory dynamics. Multi-omics-based TLS scoring and combinatorial therapies emerge as promising strategies to overcome resistance.
    Keywords:  biomarkers; gastric cancer; immune checkpoint inhibitors; progression; tertiary lymphoid structures; tumor microenvironment; tumor-infiltrating lymphocytes
    DOI:  https://doi.org/10.3389/fimmu.2025.1595070
  4. Front Immunol. 2025 ;16 1604310
    T lymphocyte heterogeneity in NSCLC: implications for biomarker development and therapeutic innovation.
    Yu Liu, Denghui Qin, Jiejun Fu.
      Non-small cell lung cancer (NSCLC) immunotherapy has been revolutionized by immune checkpoint inhibitors (ICIs), yet response heterogeneity persists due to dynamic tumor-immune interactions. This review summarizes recent studies in understanding tumor-infiltrating lymphocyte (TIL) biology, highlighting CD8+ cytotoxic T cells and regulatory T cells (Tregs) as pivotal regulators of immune surveillance and suppression. We summarize emerging biomarkers such as TCR clonality, spatial distribution of tumor-infiltrating lymphocytes (TILs), and exhaustion markers including PD-1, TCF1, and TIM-3, which predict immune checkpoint inhibitor (ICI) efficacy beyond PD-L1 expression. This review specifically describes radiotherapy-induced immunogenic remodeling and peripheral T cell dynamics as innovative strategies to monitor immune response and resistance mechanisms. By integrating results from single-cell omics and AI-driven spatial analysis, we propose multidimensional frameworks of TIL in NSCLC to overcome resistance and optimize immunotherapy combinations. These insights collectively advance NSCLC immunotherapy toward precision modulation of the tumor immune microenvironment.
    Keywords:  CD8 + T cell; NRAS mutations; PD-1; T lymphocyte; biomarkers; immunotherapy combination therapy; melanoma
    DOI:  https://doi.org/10.3389/fimmu.2025.1604310
  5. J Clin Oncol. 2025 Jun 13. JCO2402348
    Adoptive Cell Transfer of Tumor-Infiltrating Lymphocytes for Metastatic Acral Lentiginous Melanoma.
    Paul H McClelland, Shirley K Nah, Alexandra M Gustafson, Aaron J Dinerman, Bradley S White, Billel Gasmi, Donald E White, Sivasish Sindiri, Jared J Gartner, Todd D Prickett, Paul F Robbins, Maria R Parkhurst, Hyunmi Halas, Mei Li M Kwong, Stephanie L Goff, James C Yang, Steven A Rosenberg, Nicholas D Klemen.
       PURPOSE: Acral lentiginous melanoma is a subtype of cutaneous melanoma arising from palmar, plantar, or subungual skin. These tumors are characterized by aggressive biology, a low tumor mutational burden (TMB), and diminished sensitivity to immune checkpoint blockade. It is unknown whether adoptive cell transfer of tumor-infiltrating lymphocytes (ACT-TIL) has efficacy in patients with acral melanoma.
    METHODS: We analyzed prospectively collected data from 442 patients with metastatic cutaneous melanoma who were treated on clinical trials of ACT-TIL at a single institution between 1999 and 2018. Although blinded to treatment outcome and genomic data, we retrospectively identified patients who had acral subtype on the basis of clinicopathologic data available at the time of diagnosis. We then evaluated the ACT-TIL treatment outcomes of patients with acral melanoma and compared them with contemporaneously treated patients with nonacral melanoma.
    RESULTS: Out of 442 included patients, 30 (7%) had acral melanoma while 412 (93%) had nonacral melanoma. Cohorts had similar clinical characteristics, protocol enrollment, and treatment-related factors. The objective response rate to ACT-TIL in patients with acral and nonacral melanomas was 43% and 40%, respectively (P = .87), with 3% and 16% having complete responses (CRs; P = .07). Median progression-free survival was 3.5 and 4.1 months (P = .40) and median overall survival was 13 and 17 months (P = .79), respectively. Acral melanomas had lower TMB and ultraviolet mutational signature scores than nonacral melanomas.
    CONCLUSION: ACT-TIL can mediate objective responses in patients with metastatic acral melanoma, and outcomes in patients with acral disease were unexpectedly comparable with those of contemporaneously treated patients with nonacral cutaneous melanoma. Further research is necessary to understand the immunologic basis of responses to ACT-TIL in acral melanoma and to increase the frequency of CRs.
    DOI:  https://doi.org/10.1200/JCO-24-02348
  6. Int J Biol Macromol. 2025 Jun 04. pii: S0141-8130(25)05506-0. [Epub ahead of print]318(Pt 1): 144953
    Targeting B and T lymphocyte attenuator in cancer immunotherapy.
    Keywan Mortezaee.
      B and T lymphocyte attenuator (BTLA) is a co-inhibitory receptor of B7 family that shares structural homology with cytotoxic T lymphocyte associated antigen-4 (CTLA-4) and programmed death-1 (PD-1). Overlapping BTLA binding sites in herpes virus entry mediator (HVEM) for different ligand/receptor interactions including CD160 and herpes simplex virus (HSV) glycoprotein D (gD) (HSV gD) trigger competitions and provide opportunities to block one direction instead allowing the activity of another, such as LIGHT (CD258) for tumor targeted purposes. BTLA seemingly masks the therapeutic potential of anti-programmed death-1 (PD-1), so it can be a target in cancer immunotherapy. It seems that BTLA predominantly take inhibitory pro-tumor path. PD-1 mainly recruits SHP-2, while BTLA mainly recruits SHP-1 to promote immunosuppression. Targeting BTLA-HVEM ligation using BTLA inhibitors or application of peptides occupying the BTLA site in HVEM are strategies for targeting BTLA in cancer immunotherapy. However, there is also another side of the coin so that activation of growth factor receptor-bound protein 2 (Grb2) which only exists in the cytoplasmic tail of BTLA promotes stimulatory route to this checkpoint, and recalling the stimulatory path with appropriate inducers may positively affect responses to adoptive cell therapy (ACT) using tumor-infiltrating lymphocytes (TILs) against cancer.
    Keywords:  B and T lymphocyte attenuator (BTLA); Cytotoxic T lymphocyte associated antigen-4 (CTLA-4); Herpes virus entry mediator (HVEM); Programmed death-1 (PD-1); Tumor-infiltrating lymphocyte (TIL)
    DOI:  https://doi.org/10.1016/j.ijbiomac.2025.144953
  7. Mol Ther Oncol. 2025 Jun 18. 33(2): 200989
    Enhanced anti-tumor activity by zinc finger repressor-driven epigenetic silencing of immune checkpoints and TGFBR2 in CAR-T cells and TILs.
    Marion David, Phillip Schiele, Davide Monteferrario, Gaëlle Saviane, Angélique E Martelli, Coralie F Dupont, Caroline Jeanneau, Irène Marchetti, Satish K Tadi, Julia Vahldick, Lynn N Truong, Yuanyue Zhou, Igor M Sauer, Wenzel Schöning, Il-Kang Na, Andreas Reik, Marco Frentsch, Maurus de la Rosa, David Fenard.
      Chimeric antigen receptor T (CAR-T) therapies have shown remarkable success in treating hematological malignancies. However, effectiveness against solid tumors remains limited due to the immunosuppressive tumor microenvironment (TME), such as transforming growth factor β (TGF-β) signaling and upregulated immune checkpoints (ICs). Furthermore, identifying universal, tumor-specific targets for CAR-T cells in solid tumors is challenging, but using reinvigorated, immunosuppressive-resistant tumor-infiltrating lymphocytes (TILs) could be a promising alternative approach. Unlike nucleases, which may induce genotoxic DNA double-strand breaks, multiplexed zinc finger repressors (ZFRs) offer a safer alternative for knocking out TME-related immunosuppressive factors. We epigenetically repressed PD-1 expression both in CAR-T cells and TILs from colorectal liver metastases. PD-1 repression did not affect T cell viability, proliferation, or functionality. In a murine B cell lymphoma model, PD-1-repressed CD19-CAR-T cells exhibited enhanced anti-tumor activity and improved survival. Notably, PD-1 repression alone did not increase cytotoxicity against a PD-L1-positive colorectal cell line in vitro. To further increase anti-tumor potency in this context, ZFR-expressing lentiviral vectors (LVs) targeting PD-1 and other ICs (LAG-3, TIM-3, and TIGIT) or TGFBR2 were developed, improving significantly the cytotoxic activity in TILs. This strategy highlights the potential to enhance tumor-reactive T cells and improve anti-cancer immunotherapies by epigenetically repressing immunosuppressive factors in the TME using multiplexed ZFRs.
    Keywords:  CAR-T; KRAB; TILs; TME; epigenetic; immune checkpoints; repressor; zinc finger protein
    DOI:  https://doi.org/10.1016/j.omton.2025.200989
  8. J Egypt Natl Canc Inst. 2025 Jun 07. 37(1): 47
    Immunohistochemical expression of PD1, LAG3, and CTLA4 in diffuse large B cell lymphoma, clinicopathological correlation, and prognostic value.
    Madonna I William, Dina A Tantawy, Alyaa R Elsergany, Amira K El-Hawary, Shaimaa M Yussif.
       BACKGROUND: The tumor microenvironment has an important role in the growth and progression of diffuse large B-cell lymphoma (DLBCL). Immune checkpoint molecules, including PD1, LAG3, and CTLA4, are crucial to regulate the T cells function in the tumor microenvironment. Exploring the expression of these molecules in DLBCL microenvironment is crucial for developing targeted therapies enhancing anti-tumor immune responses.
    AIM: This study aims to evaluate the immunohistochemical (IHC) expression of PD1, LAG3, and CTLA4 in DLBCL, assess the relation of their expression to different clinicopathological parameters and evaluate their prognostic significance.
    METHODS: This retrospective study encompassed 103 cases diagnosed as de novo DLBCL. Clinicopathologic and survival data were gathered. IHC for PD1, LAG3, and CTLA4 was performed.
    RESULTS: PD1, LAG3, and CTLA4 positive reaction was observed in tumor-infiltrating lymphocytes (TILs) in 68.9% (71/103), 82.5% (85/103), and 92.2% (95/103) of DLBCL cases, respectively. PD1 expression in TILs was significantly associated with hepatitis C virus (HCV) positivity and prolonged overall survival (OS) in univariate analysis. LAG3 expression in TILs was significantly associated with IPI score and tended towards shorter OS (not statistically significant). LAG3 expression in tumor cells was significantly associated with shorter disease-free survival (DFS). CTLA4 expression in TILs was significantly associated with advanced disease stage (III/IV).
    CONCLUSION: PD1 and LAG3 are expressed mainly in TILs. PD1 expression (in TILs and tumor cells) is associated with prolonged OS, while LAG3 expression (in tumor cells) is associated with shorter DFS and its expression in TILs tended towards shorter OS. CTLA4 expression is associated with advanced disease stage but not associated with OS. These findings may suggest that immune checkpoint inhibitors targeting LAG3 may offer therapeutic potential in DLBCL by enhancing the antitumor immune response. Additional research is needed to assess the effectiveness of inhibition of these checkpoint molecules in combination with existing treatment modalities.
    Keywords:  CTLA4; DLBCL; LAG3; PD1; Survival
    DOI:  https://doi.org/10.1186/s43046-025-00303-0
  9. Breast Cancer Res Treat. 2025 Jun 09.
    Tumoral pSMAD2 as a prognostic biomarker in early-stage breast cancer: insights from the randomized SweBCG91RT trial.
    Axel Stenmark Tullberg, Viktoria Thurfjell, Anikó Kovács, Patrick Micke, Aristidis Moustakas, Fredrika Killander, Emma Niméus, Erik Holmberg, Per Karlsson, Carina Strell.
       BACKGROUND/AIM: The TGF-β pathway can influence breast cancer progression and therapy efficacy, exhibiting both pro- and anti-tumoral effects. This study examined the impact of active TGF-β signaling on recurrence and radiotherapy (RT) benefit in early-stage breast cancer, using nuclear phosphorylated Smad2 (pSMAD2) as a marker for pathway activation.
    METHODS: Tissue-microarrays from 1178 stage I-IIA breast cancer patients in the SweBCG91RT trial (randomized to breast-conserving surgery with or without RT) were analyzed. pSMAD2 immunohistochemistry was scored as the mean percentage of tumor cells with nuclear staining. Recurrence risk and RT benefit were evaluated.
    RESULTS: pSMAD2 scores were heavily skewed, with 45% of tumors demonstrating high staining (≥ 80% tumor cells), 38% medium (21-79%), and 17% low (≤ 20%). Low pSMAD2 tumors were associated with higher grade and larger size but not with subtype. Medium pSMAD2 tumors had a significantly increased ipsilateral breast tumor recurrence risk than high pSMAD2 tumors (HRadjusted = 1.82, p = 0.002), while no differences were observed for low pSMAD2 tumors. A similar result was obtained with all recurrences as endpoint. RT benefit was consistent across all pSMAD2 groups. In Luminal tumors, higher tumoral pSMAD2 levels were inversely correlated with tumor-infiltrating lymphocytes (TILs).
    CONCLUSION: Medium pSMAD2 levels were linked to an increased recurrence risk compared to high levels, suggesting a tumor-suppressive role of TGF-β in early breast tumorigenesis. However, no significant differences were noted for low pSMAD2 levels. In Luminal tumors, TGF-β signaling was negatively associated with TILs. These findings indicate that therapeutic targeting of TGF-β warrants careful consideration of tumor stage and subtype.
    Keywords:  Breast cancer; Immune cells; Prognosis; Radiotherapy; SMAD2; TGF-β signaling
    DOI:  https://doi.org/10.1007/s10549-025-07744-0
  10. Semin Oncol. 2025 Jun 06. pii: S0093-7754(25)00062-4. [Epub ahead of print]52(4): 152370
    CTLA-4 blockade in ovarian cancer immunotherapy: Mechanisms and clinical strategies.
    Chou-Yi Hsu, Thikra Majid Muhammed, Subasini Uthirapathy, Irfan Ahmad, Suhas Ballal, Rishiv Kalia, Premkumar J, Subhashree Ray, Riyadh Mohammed Mohsin, Abid ALi A Abiess.
      Although studies have demonstrated that ovarian cancer cells can express immune checkpoint proteins like CTLA-4 and that higher levels of tumor-infiltrating lymphocytes are linked to better patient survival, clinical trials utilizing immune checkpoint inhibitors in ovarian cancer have not yielded encouraging results. Tumor heterogeneity and innate or acquired resistance associated with the tumor microenvironment (TME) may account for the inadequate response to ICIs. Understanding tumor immunobiology, identifying biomarkers for patient selection, and formulating suitable treatment regimens remain challenging, yet these are the aspirations for the future use of immunotherapy in ovarian cancer. Induced T cells express CD80 and CD86, providing a positive costimulatory signal via CD28. CTLA-4 antagonizes CD28, diminishing T cell activation and modulating the immunological response. Conversely, the negative regulation of CTLA-4 using monoclonal antibodies (mAbs), particularly ipilimumab, may stimulate T-cell responses against ovarian cancer antigens. We elucidate the mechanisms responsible for immunological suppression: T cell exhaustion and senescence in ovarian cancer. We also provide a synopsis of using CTLA-4 monoclonal antibodies in ovarian cancer alone or conjunction with other modalities (eg, chemotherapy). We finally delineate the challenges associated with responding to immunotherapy in ovarian cancer.
    Keywords:  CTLA-4; Immunotherapy; Ipilimumab; Ovarian cancer; Tumor microenvironment
    DOI:  https://doi.org/10.1016/j.seminoncol.2025.152370
  11. Int J Surg. 2025 Jun 10.
    Intratumoral IL-33 + CD4 + FoxP3 + regulatory T cell infiltration determines poor clinical outcomes and intensive immunoevasive contexture in patients with pancreatic cancer after surgical resection: a cohort study.
    Ning Pu, Qiangda Chen, Jiande Han, Zhihang Xu, Zhenlai Jiang, Taochen He, Yanfei An, Yaolin Xu, Wei Gan, Haibo Wang, Wenquan Wang, Wenchuan Wu, Yun Jin, Jun Yu, Wenhui Lou, Hanlin Yin, Liang Liu.
       BACKGROUND: Interleukin-33 (IL-33), a member of the IL-1 cytokine family, is constitutively expressed in barrier cells such as endothelial cells and fibroblasts. While the expression of IL-33 in regulatory T cells (Tregs) has been previously reported, its clinical significance in pancreatic ductal adenocarcinoma (PDAC) remains unclear. This study aims to investigate the clinical relevance and biological role of IL-33 + Tregs in PDAC.
    METHODS: Infiltration of IL-33 + Tregs was assessed by immunohistochemistry in 215 patients from our institute. The correlation between IL-33 + Tregs and clinical characteristics was analyzed. Additionally, the functional status of cytotoxic T cells in relation to IL-33 + Treg infiltration was examined. The impact of IL-33 + Tregs on the tumor microenvironment (TME) was further evaluated both in silico and in vitro .
    RESULTS: IL-33 + Tregs infiltration was confirmed in PDAC tissues, and its abundance was positively associated with microvascular invasion, perineural invasion, and elevated serum CA19-9 levels. Patients with higher tumor-infiltrating IL-33 + Tregs demonstrated poorer overall survival (OS) and recurrence-free survival (RFS) compared to those with lower infiltration levels. Multivariate analysis confirmed IL-33 + Tregs as an independent prognostic factor for both OS and RFS, with improved survival prediction when combined with tumor differentiation. Subgroup analyses indicated that serum CA19-9 was not a useful risk stratification tool in patients with high IL-33 + Treg infiltration, and these patients showed limited survival benefit from adjuvant chemotherapy. Furthermore, increased IL-33 + Treg infiltration was associated with more pronounced immunosuppressive TME, marked by a reduction in cytotoxic phenotypes and an upregulation of exhausted markers on CD8 + T cells.
    CONCLUSION: Our findings identify IL-33 + Tregs as a novel subtype of Tregs, with strong prognostic value for survival risk stratification and therapeutic response prediction in PDAC. IL-33 + Tregs exhibit more pronounced immunosuppressive capabilities, impairing CD8 + T cell function. With further investigation, IL-33 + Tregs may represent a promising immunotherapeutic target for PDAC.
    Keywords:  IL-33; immunotherapy; pancreatic ductal adenocarcinoma; prognosis; regulatory T cells; tumor microenvironment
    DOI:  https://doi.org/10.1097/JS9.0000000000002733
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