Exhaustion of tumor-specific CD8⁺ T cells in metastases from melanoma patients.
By L. Baitsch, Petra Baumgaertner, Estelle F. Devêvre, S. Raghav, A. Legat, L. Barba, Sébastien Wieckowski, H. Bouzourène, B. Deplancke, P. Romero and 2 more. Journal of Clinical Investigation, 2011
832 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/8f42b65b884205bda1f95dea00fdb8084f9d297c
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In Immunology
- Erika L. Pearce
- S. Rosenberg
- Ton N. Schumacher
- A. Schietinger
- Michael D. Buck
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- M. Dudley
- D. Thommen
In Oncology
- S. Rosenberg
- Ton N. Schumacher
- M. Dudley
- D. Thommen
- A. Schietinger
- P. Greenberg
- Kristen E. Pauken
- Jie Yang
Citations in the corpus
- Dissecting the multicellular ecosystem of metastatic melanoma by single-cell RNA-seq (2016, neutral): “Three independently derived exhaustion gene-sets were used to define high and low exhaustion cells (Mel75, (17, 46, 48)), and the corresponding results are represented as distinct columns for each tumor.”
- Adoptive immunotherapy for cancer: harnessing the T cell response (2012, neutral): “TIL’ler organizma içinde (in vivo) T hücresi immunoglobulini, müsin alt birimi (mucin domain) içeren protein 3 (TIM3), lenfosit aktivasyonu gen 3 proteini (LAG3), programlanmış hücre ölümü proteini 1 (PD1) ve sitotoksik T lenfositi antijeni 4 (CTL4) gibi bağışıklık baskılayıcı moleküllerce engelleni”
- PD-1 identifies the patient-specific CD8⁺ tumor-reactive repertoire infiltrating human tumors. (2014, background): “This altered phenotype, and the interaction of these receptors with their corresponding ligands on target cells, is associated with impaired proliferation and effector function frequently referred to as exhaustion (18, 24, 40).”
- T Cell Dysfunction in Cancer (2018, background): “…metastases after vaccination largely overlaps with the exhaustion signature derived from CD8+ T cells during chronic LCMV infection, and contains similar alterations in processes involved in immune response, cell migration, signaling, metabolism, cell cycle, and DNA repair (Baitsch et al., 2011).”
- Tumor-Specific T Cell Dysfunction Is a Dynamic Antigen-Driven Differentiation Program Initiated Early during Tumorigenesis (2016, positive): “We therefore compared the gene signature of D8 and D34 TCRSV40-I with that of T cells from late-stage human tumors using the transcriptional profiles of tumor-reactive human Mart-1/Melan-A-specific CD8 T cells isolated from metastases of melanoma patients (Figures 4A, top, and S4; Baitsch et al., 20”
- T cell costimulatory receptor CD28 is a primary target for PD-1–mediated inhibition (2016, background): “The interaction between PD-1 and its ligands also has been shown to restrain effector T cell activity against human cancers (10-14).”
- Overcoming T cell exhaustion in infection and cancer (2015, background): “Lastly, transcriptional profiling comparing Melan-A/MART-1 tumorspecific CD8+ T cells in metastases from melanoma patients to gp33 virus-specific TEX cells in chronic LCMV infection showed substantial overlap in the molecular program of these populations [78].”
- Anti-PD-1 and Anti-CTLA-4 Therapies in Cancer: Mechanisms of Action, Efficacy, and Limitations (2018, background): “Originally described in the context of chronic viral infections, where the host fails to clear the pathogen, it is now apparent that exhausted T cells can also occur in cancer (12, 13).”