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Homo sapiens

ABSTRACT: CD4+ and CD8+ tumor-infiltrating lymphocytes in breast cancer

PROVIDER: PRJNA925311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23121100_1.fastq.gz	Fastqsanger.gz
	SRR23121100_2.fastq.gz	Fastqsanger.gz
	SRR23121101_1.fastq.gz	Fastqsanger.gz
	SRR23121101_2.fastq.gz	Fastqsanger.gz
	SRR23121102_1.fastq.gz	Fastqsanger.gz

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The transcription factor BACH2 is required to establish immunosuppression within tumors

Project description:Through a diversity of functional lineages, cells of the innate and adaptive immune system either drive or constrain immune reactions within tumors. Thus, while the immune system has a powerful ability to recognize and kill cancer cells, this function is often suppressed preventing clearance of disease. The transcription factor (TF) BACH2 controls the differentiation and function of multiple innate and adaptive immune lineages, but its role in regulating tumor immunity is not known. Here, we demonstrate that BACH2 is required to establish immunosuppression within tumors. We found that growth of subcutaneously implanted tumors was markedly impaired in Bach2-deficient mice and coincided with intratumoral activation of both innate and adaptive immunity but was dependent upon adaptive immunity. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-Î³. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression. These findings demonstrate that BACH2 is a key component of the molecular programme of tumor immunosuppression and identify a new target for development of therapies aimed at reversing immunosuppression in cancer. Analysis of tumor-infiltrating lymphocytes in Bach2-deficient mice revealed high frequencies of CD4+ and CD8+ effector cells expressing the inflammatory cytokine IFN-Î³. Lymphocyte activation coincided with reduction in the frequency of intratumoral CD4+ Foxp3+ regulatory T (Treg) cells. Mechanistically, Treg-dependent inhibition of CD8+ T cells was required for BACH2-mediated tumor immunosuppression.

2016-06-01 | E-GEOD-74653 | biostudies-arrayexpress

Gene expression data of CD8+ T cells from C57BL/6 mouse

Project description:Anti-CD4 monoclonal antibody, a prominent immunomodulatory agent, elicits robust anti-tumor immunity in various cancers by increasing tumor-infiltrating lymphocytes and promoting CD8+ T cell reactivity against tumor cell-derived antigens. We used microarrays to investigate anti-CD4-induced gene-expression change of CD8+ T cells.

2021-07-18 | GSE180291 | GEO

Homo sapiens

Project description:Non-cancerous liver infiltrating lymphocytes of hepatitis C and tumor-infiltrating lymphocytes

| PRJNA108017 | ENA

FcγRIIB engagement drives agonistic activity of Fc-engineered αOX40 antibody to stimulate human tumor-infiltrating T cells

Project description:Background: OX40 (CD134) is a co-stimulatory molecule of the tumor necrosis factor receptor (TNFR) superfamily, that is currently investigated as a target for cancer immunotherapy. However, despite promising results in murine tumor models, the clinical efficacy of agonistic αOX40 antibodies in treatment of cancer patients has fallen short of the high expectation in earlier stage trials. Methods: Using lymphocytes from resected tumor, tumor-free tissue and PBMC of 4 hepatocellular and colorectal cancer patients, we performed RNA-Seq to evaluate OX40-mediated transcriptional changes in CD4+ and CD8+ human tumor-infiltrating lymphocytes (TILs). Results: The transcriptional landscape of CD4+ and CD8+ TILs shifted towards a pro-survival, inflammatory and chemotactic profile upon treatment with αOX40_v12.

2020-06-22 | GSE152904 | GEO

Anti-CD4 treatment affects TCR repertoire of CD8+ T cells

Project description:Anti-CD4 monoclonal antibody, a prominent immunomodulatory agent, elicits robust anti-tumor immunity in various cancers by increasing tumor-infiltrating lymphocytes and promoting CD8+ T cell reactivity against tumor cell-derived antigens. We conducted TCR repertoire analysis of anti-CD4-exposed endogenous CD8+ T cells to investigate the expansion pattern of the cell population.

2021-08-03 | GSE181280 | GEO

Anti-CD4 treatment increases tumor-suppressive IL18Rαhi CD8+ T cells

Project description:Anti-CD4 monoclonal antibody, a prominent immunomodulatory agent, elicits robust anti-tumor immunity in various cancers by increasing tumor-infiltrating lymphocytes and promoting CD8+ T cell reactivity against tumor cell-derived antigens. We conducted single-cell transcriptome analysis of anti-CD4-exposed lymphoid cells to investigate the detailed mechanism.

2021-07-30 | GSE180991 | GEO

Homo sapiens

Project description:Human CD28+/- tumor infiltrating lymphocytes gene expression

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PD-L1 overexpression, SWI/SNF complex Deregulation and Profound Transcriptomic Changes Characterize Cancer-Dependent Exhaustion of Persistently Activated CD4+ T Cells

Project description:The growing tumor avoids recognition and destruction by immune system. During continuous stimulation of tumor infiltrating lymphocytes (TILs) by tumor, TILs become functionally exhausted. Thus, they become unable to kill tumor cells and to produce some cytokines, and lose their ability to proliferate. It collectively results in the immune escape of cancer cells. Here, we show that breast cancer cells expressing PD-L1 can accelerate exhaustion of persistently activated human effector CD4+ T cells, manifesting in high PD-1 and PD-L1 expression level on cell surface, decreased glucose metabolism genes, strong downregulation of SWI/SNF chromatin remodeling complex subunits and p21 cell cycle inhibitor upregulation. This results in inhibition of T cell proliferation and reduction of T cells number. The RNAseq analysis on exhausted CD4+ T cells indicated strong overexpression of IDO1 and genes encoding pro-inflammatory cytokines and chemokines. The PD-L1 overexpression was also observed in CD4+ T cells after co-cultivation with other cell line overexpressing PD-L1 that suggested the existence of general mechanism of CD4+ T cell exhaustion induced by cancer cells. The ChIP analysis on PD-L1 promoter region indicated that the strong BRM recruitment in control CD4+ T cells is replaced by BRG1 and EZH2 in CD4+ T cells strongly exhausted by cancer cells. These findings suggest that such epi-drugs as EZH2 inhibitors may be used as immunomodulators in cancer treatment.

2022-02-17 | PXD026447 | Pride

Homo sapiens

Project description:Expression data from FACS-sorted CD8+BTLA+ vs CD8+BTLA- Human Tumor-infiltrating Lymphocytes in Metastatic Melanoma

| PRJNA185170 | ENA

Homo sapiens

Project description:Tumor-infiltrating lymphocytes, prognosis and trastuzumab benefit in early-stage breast cancer patients from the FinHER trial

| PRJNA208626 | ENA