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RNAseq analysis of anti-BTLA vs control treated anti-CD3 stimulated mouse T cells or IgM stimulated mouse B cells

ABSTRACT: This dataset comprises an analysis of BTLA signaling in wild-type mouse T cells or B cells. These purified CD4+ T cells or purified B cells were stimulataed through their antigen receptors and/or Interferon receptor and costimulated with anti-BTLA mAb that activates BTLA signaling. High throughput sequencing was performed on the RNA purified from stimulated populations to characterize how BTLA signaling regulates antigen receptor and type I interferon receptor signaling in T cells and B cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE196204 | GEO | 2022/02/09

REPOSITORIES: GEO

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Analysis of BTLA regulated transcripts in human B and CD4+ T cells

Project description:Purified B or CD4+ T cells were analyzed for transcriptional changes induced by the BTLA inhibitory receptor. BTLA receptors were activated using anti-human BTLA coupled to microbeads. Gene expression was analyzed using Nanostring

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

Project description:Adoptive T-cell Therapy (ACT) involves using tumor-infiltrating lymphocytes (TIL) isolated from metastatic melanoma and expanding them ex vivo prior to infusion into lympho-depleted patients. This is one of the most promising approaches to treat metastatic melanoma, with the rates of clinical response between 48-50% based on studies done at NCI, M.D. Anderson Cancer Center (Houston, TX), and Sheba Medical Center (Tel Aviv, Israel). In the Phase II ACT Trial at M.D. Anderson Cancer Center , our group has uncovered an association between positive clinical response and the amount of CD8+ tumor-infiltrating lymphocytes expressing B and T Lymphocyte Attenuator (BTLA), a reported inhibitory receptor on T-cells. We used microarrays to detail the differences in the global programme of gene expression between CD8+BTLA+ vs CD8+BTLA- TILs in order to understand the molecular basis of the clinical association. TILs were isolated by enzymatically digest the melanoma tumor fragments obtained from Stage IIIc/IV melanoma patients at M.D. Anderson Cancer Center. The TILs were expanded with high-dose IL-2 for two weeks prior to sorting by FACS (fluoresecence-activated cell sorter) for CD8+BTLA+ and CD8+BTLA- susbets. RNA was extracted from each sorted subsets and hybridized on Affymetrix microarrays

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Regulation of Intestinal microbiome diversity by BTLA and HVEM

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Tumor cell-intrinsic BTLA receptor inhibits the proliferation of tumor cells via ERK1/2

Project description:B and T lymphocyte attenuator (BTLA) is an immune checkpoint molecule that mediates the escape of tumor cells from immunosurveillance. Consequently, BTLA and its ligand-herpesvirus entry mediator （HVEM） are potentially immunotherapeutic targets. However, the potential effects of BTLA on tumor cells remain incompletely unknown. Here, we show that BTLA is expressed across a broad range of tumor cells. The depletion of BTLA or HVEM promotes cell proliferation and colony formation，which is reversed by re-overexpression of BTLA in BTLA knockout (KO) cells. On the contrary, overexpression of BTLA or HVEM inhibits tumor cell proliferation and colony formation. Furthermore, the proliferation of subpopulation with high BTLA is also significantly slower than that of the low BTLA subpopulation. Mechanistically, the coordination of BTLA and HVEM inhibits its major downstream ERK1/2 signaling pathway, thus preventing tumor cell growth. This study demonstrates that tumor cell-intrinsic BTLA/HVEM is a potential tumor suppressor and likely to have potential antagonist for immunotherapy, thus representing a potential biomarker for the optimal cancer immunotherapeutic treatment.

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