CD8+ Tumor-Infiltrating Lymphocyte Abundance is a Positive Prognostic Indicator in Nasopharyngeal Cancer
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ABSTRACT:
PROVIDER: EGAS00001006396 | EGA |
REPOSITORIES: EGA
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Project description:A retrospective tissue study to explore the prognostic significance of tumor-infiltrating lymphocyte (TIL) populations in Nasopharyngeal Cancer, using a combination of RNA sequencing and immunohistochemistry.
2022-09-01 | E-MTAB-11963 | biostudies-arrayexpress
Project description:We had previously demonstrated the role of CD103 integrin on lung tumor-infiltrating lymphocyte (TIL) clones in promoting specific TCR-mediated epithelial tumor cell cytotoxicity. However, the contribution of CD103 on intratumoral T-cell distribution and functions, and the prognosis significance of TIL subpopulations in non-small cell lung carcinoma (NSCLC) have thus far not been systematically addressed. Here we investigate the transcriptomic profil of these cell population, using PBMC cells as control.
2015-06-29 | E-MTAB-3266 | biostudies-arrayexpress
Project description:Tumors that contain tumor-infiltrating lymphocytes (TIL) with tissue-resident memory T cells (TRM) features are associated with better patient prognoses. While CD8+ T cells that target tumors often fail to restrain tumor growth due to progressive T cell exhaustion, pathogen-specific TRM survey tissues and sustain protective capacity for years. We identified protein homeostasis (proteostasis)-related E3 ubiquitin ligase genes shared by TRM and progenitor-exhausted TIL (TPEX), that are lost as TIL become terminally-exhausted (TEX). Sustained ligase expression led to increased TCF1+ T cell accumulation and improved anti-tumor function and less T cell exhaustion in chronic infection. Loss-of-function in cancer models impaired TIL accumulation and function and altered T cell differentiation in response to acute infection. Low-input mass spectrometry revealed abundant expression of protein degradation pathways by TEX, yet they accumulated unfolded proteins. Ligase overexpression rescued unfolded protein accumulation in TEX, demonstrating their functional contribution to proteostasis. Ligase overexpression in combination with immune checkpoint blockade led to improved survival from murine melanoma, demonstrating that the relationship between proteostasis and T cell differentiation opens up new avenues for cancer immunotherapy.
2026-04-21 | PXD063865 | Pride
Project description:Tumors that contain tumor-infiltrating lymphocytes (TIL) with tissue-resident memory T cells (TRM) features are associated with better patient prognoses. While CD8+ T cells that target tumors often fail to restrain tumor growth due to progressive T cell exhaustion, pathogen-specific TRM survey tissues and sustain protective capacity for years. We identified protein homeostasis (proteostasis)-related E3 ubiquitin ligase genes shared by TRM and progenitor-exhausted TIL (TPEX), that are lost as TIL become terminally-exhausted (TEX). Sustained ligase expression led to increased TCF1+ T cell accumulation and improved anti-tumor function and less T cell exhaustion in chronic infection. Loss-of-function alleles in T cells challenged with cancer models impaired TIL accumulation and function and altered T cell differentiation in response to acute infection. Mass spectrometry revealed abundant expression of protein degradation pathways by TEX, yet they accumulated unfolded proteins. Ligase overexpression rescued unfolded protein accumulation in TEX, demonstrating their functional contribution to proteostasis. Ligase overexpression in combination with immune checkpoint blockade led to improved survival from murine melanoma, demonstrating that the relationship between proteostasis and T cell differentiation opens up new avenues for cancer immunotherapy.
2026-04-30 | PXD067417 | Pride
Project description:Tumors that contain tumor-infiltrating lymphocytes (TIL) with tissue-resident memory T cells (TRM) features are associated with better patient prognoses. While CD8+ T cells that target tumors often fail to restrain tumor growth due to progressive T cell exhaustion, pathogen-specific TRM survey tissues and sustain protective capacity for years. We identified protein homeostasis (proteostasis)-related E3 ubiquitin ligase genes shared by TRM and progenitor-exhausted TIL (TPEX), that are lost as TIL become terminally-exhausted (TEX). Sustained ligase expression led to increased TCF1+ T cell accumulation and improved anti-tumor function and less T cell exhaustion in chronic infection. Loss-of-function in cancer models impaired TIL accumulation and function and altered T cell differentiation in response to acute infection. Low-input mass spectrometry revealed abundant expression of protein degradation pathways by TEX, yet they accumulated unfolded proteins. Ligase overexpression rescued unfolded protein accumulation in TEX, demonstrating their functional contribution to proteostasis. Ligase overexpression in combination with immune checkpoint blockade led to improved survival from murine melanoma, demonstrating that the relationship between proteostasis and T cell differentiation opens up new avenues for cancer immunotherapy.
2026-04-21 | PXD070932 | Pride
Project description:420 locoregionally advanced NPC patients underwent pEBV DNA screening. 156 patients (37.1%) who had pEBV DNA ≥4000 copies/mL were included and randomly assigned to CCRT plus TIL infusion group (n=78) and CCRT alone group (n=78). Outcomes were classified as patients with a poor outcome (nonresponders) and patients with a favorable outcome (responders). Single cell RNA sequencing (scRNA-seq) for infused TIL products in responder and non-responder.
2024-06-30 | GSE179224 | GEO
Project description:CD8+ tumor-infiltrating lymphocytes (TIL) often fail to restrain tumor growth due to differentiation to T cell exhaustion. In healthy tissues, tissue-resident memory T cells (TRM) survey tissues and sustain protective capacity for years, and tumors that contain TIL with TRM-features are associated with better patient prognosis. We identified protein homeostasis (proteostasis) significant in distinguishing TRM and progenitor-exhausted TIL (TPEX) from terminally-exhausted TIL (TEX) by identifying multiple E3 ubiquitin ligases that maintain T cell differentiation potential. Sustained ligase-expression in TIL enhanced T cell accumulation, preserved stem-like TCF1+ populations, and improved anti-tumor function, whereas ligase loss-of-function impaired TIL and altered T cell differentiation in acute infection. TEX experience a loss of proteostasis, marked by unfolded protein accumulation despite functional proteasomes. Enforced ligase expression rescued this unfolded protein accumulation in TIL and improved immunotherapy responses, demonstrating the role of proteostasis in maintaining differentiation potential and identifying new avenues for advancing cancer immunotherapies.
2026-04-22 | GSE298128 | GEO
Project description:CD8+ tumor-infiltrating lymphocytes (TIL) often fail to restrain tumor growth due to differentiation to T cell exhaustion. In healthy tissues, tissue-resident memory T cells (TRM) survey tissues and sustain protective capacity for years, and tumors that contain TIL with TRM-features are associated with better patient prognosis. We identified protein homeostasis (proteostasis) significant in distinguishing TRM and progenitor-exhausted TIL (TPEX) from terminally-exhausted TIL (TEX) by identifying multiple E3 ubiquitin ligases that maintain T cell differentiation potential. Sustained ligase-expression in TIL enhanced T cell accumulation, preserved stem-like TCF1+ populations, and improved anti-tumor function, whereas ligase loss-of-function impaired TIL and altered T cell differentiation in acute infection. TEX experience a loss of proteostasis, marked by unfolded protein accumulation despite functional proteasomes. Enforced ligase expression rescued this unfolded protein accumulation in TIL and improved immunotherapy responses, demonstrating the role of proteostasis in maintaining differentiation potential and identifying new avenues for advancing cancer immunotherapies.
2026-04-22 | GSE298127 | GEO
Project description:The subject of this study is the adoptive transfer of selected autologous tumor infiltrating lymphocytes (TIL) after in vitro expansion for the treatment of solid tumor malignancies. The TIL selection process is based on evidence showing that CD8+ TIL which co-express both CD39 and CD103 harbor the bulk of tumor-reactivity and that the remaining CD8 TIL is mainly composed of non-tumor reactive bystander cells. All of the expanded TIL that are produced (1-40 billion are expected) will be delivered in the form of a cell suspension to the participants by intravenous infusion. It is proposed that these selected TIL will produce a more potent and efficacious treatment of late-stage cancer.
| 63320 | ecrin-mdr-crc
Project description:Adoptive cell therapy (ACT) using ex vivo–expanded tumor-infiltrating lymphocytes (TILs) can eliminate or shrink metastatic melanoma, but its long-term efficacy remains limited to a fraction of patients. Using longitudinal samples from 13 patients with metastatic melanoma treated with TIL-ACT in a phase 1 clinical study, we interrogated cellular states within the tumor microenvironment (TME) and their interactions. We performed bulk and single-cell RNA sequencing, whole-exome sequencing, and spatial proteomic analyses in pre- and post-ACT tumor tissues, finding that ACT responders exhibited higher basal tumor cell–intrinsic immunogenicity and mutational burden. Compared with nonresponders, CD8+ TILs exhibited increased cytotoxicity, exhaustion, and costimulation, whereas myeloid cells had increased type I interferon signaling in responders. Cell-cell interaction prediction analyses corroborated by spatial neighborhood analyses revealed that responders had rich baseline intratumoral and stromal tumor–reactive T cell networks with activated myeloid populations. Successful TIL-ACT therapy further reprogrammed the myeloid compartment and increased TIL-myeloid networks. Our systematic target discovery study identifies potential T-myeloid cell network–based biomarkers that could improve patient selection and guide the design of ACT clinical trials.
2024-02-05 | GSE222750 | GEO