Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Gene expression profiles of antigen-specific CD4+ T cells from mice carrying T cell-specific deletions of MyD88 or IL6Ra

ABSTRACT: 2W:I-A(b) specific CD4+ T cells were isolated from immunized knock-out mice and wild-type controls on day 7 post immunization and the gene expression profiles of the cells were compared Antigen-specifc CD4+ T cells were isolated and pooled from 4 independent experiments. The samples represent antigen-specific T cells from 15-30 mice per genotype.

ORGANISM(S): Mus musculus

SUBMITTER: Dominik Schenten

PROVIDER: E-GEOD-56966 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Signaling through the adaptor molecule MyD88 in CD4+ T cells is required to overcome suppression by regulatory T cells.

Schenten Dominik D Nish Simone A SA Yu Shuang S Yan Xiting X Lee Heung Kyu HK Brodsky Igor I Pasman Lesley L Yordy Brian B Wunderlich F Thomas FT Brüning Jens C JC Zhao Hongyu H Medzhitov Ruslan R

Immunity 20140101 1

Innate immune recognition controls adaptive immune responses through multiple mechanisms. The MyD88 signaling adaptor operates in many cell types downstream of Toll-like receptors (TLRs) and interleukin-1 (IL-1) receptor family members. Cell-type-specific functions of MyD88 signaling remain poorly characterized. Here, we have shown that the T cell-specific ablation of MyD88 in mice impairs not only T helper 17 (Th17) cell responses, but also Th1 cell responses. MyD88 relayed signals of TLR-induc ...[more]

PMID: 24439266

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Project description:Tumors express a wide variety of both mutated and non-mutated antigens. Whether these tumor antigens are broadly recognized as âselfâ or âforeignâ by the immune system is currently unclear. Using an autochthonous prostate cancer model in which hemagglutinin (HA) is specifically expressed in the tumor (ProHA x TRAMP mice), as well as an analogous model wherein HA is expressed in normal tissues as a model self-antigen (C3HAHigh), we examined the transcriptional profile of CD4 T cells undergoing antigen-specific division. Consistent with our previous data, transfer of antigen-specific CD4 T cells into C3HAHigh resulted in a functionally inactivated CD4 T cell profile. Conversely, adoptive transfer of an identical CD4 T cell population into ProHA x TRAMP resulted in the induction of a regulatory phenotype (Treg) both at the transcriptional and functional level. Interestingly, this Treg skewing was a property of even early-stage tumors, suggesting Treg induction as an important tolerance mechanism during tumor development. The goal of this microarray is to detail the transcriptional profile differences between CD4 T cells that recognize their cognate antigen in the context of tumor (ProHA x TRAMP model) or self-antigen recognition (C3HA) or viral-antigen recognition (VaccHA) models or unprimed naÃ¯ve state (Nontransgenic). The comparison contains both upregulated and downregulated transcripts. Experiment Overall Design: TCR transgenic CD4 T cells specific for hemagglutinin (HA) were adoptively transferred into tumor-antigen recognition model (ProHA x TRAMP), Self-antigen recognition model (C3HA), viral-antigen recognition model (VaccHA), and naÃ¯ve control (Nontrangenic). Divided (CFSE diluted) CD4 T cells were sorted by FACS, RNA was extracted, and biological replicated were hybridized to an Affymetrix Mouse 430 Plus 2 expression array, followed by interrogation with an Affymetrix GeneChip Scanner 3000. RMA normalization was employed to identify differentially expressed transcripts.

Dataset Information

Gene expression profiles of antigen-specific CD4+ T cells from mice carrying T cell-specific deletions of MyD88 or IL6Ra

Publications

Signaling through the adaptor molecule MyD88 in CD4+ T cells is required to overcome suppression by regulatory T cells.

Similar Datasets

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