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Transcriptome analysis of Th2 CD4+ T cells differentiated from wild-type and NLRP3KO mice

ABSTRACT: We report that the Th2 differentiation program is altered in absence of NRLP3 protein

ORGANISM(S): Mus musculus

PROVIDER: GSE54561 | GEO | 2015/05/12

SECONDARY ACCESSION(S): PRJNA237035

REPOSITORIES: GEO

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Transcriptome analysis of Th2 CD4+ T cells differentiated from wild-type and NLRP3KO mice

Project description:We report that the Th2 differentiation program is altered in absence of NRLP3 protein Examination of the expression profile of Th2 CD4+ T cells after 3 and 6 days of differentiation

2015-05-12 | E-GEOD-54561 | biostudies-arrayexpress

Transcriptome analysis of TH2 CD4(+) T cells differentiated from wild-type and NLRP3KO mice.

Project description:The Nod-like receptor NLRP3 is involved in the formation of NLRP3. Up to now, the immunological functions of NLRP3 independently of inflammasome is unclear. In this dataset containing 6 samples (TH0, TH2 cells at day 3 and day 6 in wild type or Nlrp3 deficient cells), we show that NLRP3 expression in CD4(+) T cells supports a T helper 2 (TH2) transcriptional program in a cell-intrinsic manner (raw and normalized data are accessible on Gene Expression Omnibus database under the number GSE54561, http://www.dtd.nlm.nih.gov/geo/query/acc.cgi?acc=GSE54561). Indeed, NLRP3 positively-regulated TH2 program independently of inflammasome formation. These data indicated that TH2 specific genes such as cMaf or Il4 were not induced in Nlrp3 deficient cells. These results demonstrate the capacity of NLRP3 to act as a key transcription factor in TH2 differentiation.

| S-EPMC4583695 | biostudies-literature

Transcriptome analysis of CD4+ T cells differentiated from wild-type and CD4cre IRF8flox mice

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Transcriptome analysis of Bcl11b-deficient CD4+ T-cells during Th2 immune response

Project description:Naïve CD4+ T-helper cells differentiate into Th2 effector cells during asthma and helminth (worm) infection. Here, we report that mice lacking the transcription factor Bcl11b in mature CD4+ T-cells are incapable of mounting an effective Th2 response in asthma and worm infection, with a major reduction of Th2 cytokine secretion and GATA3 expression. We found that Bcl11b exerts its role in Th2 differentiation through several avenues: (1) association with intronic regions at the Gata3 locus, sustaining GATA3 expression; (2) binding to and restricting chromatin accessibility at the Il4 silencer, located at hypersensitivity site (HS) IV; and (3) restricting Runx3 expression by association with a regulatory region 5’ of Runx3. Thus, in the absence of Bcl11b, the reduction in GATA3 levels combined with increased Runx3 levels and activity at Il4 HS IV silencer and consequently diminished IL-4 expression. This results in reduced chromatin opening at the Th2 locus control region (LCR), Il13 and Il5 promoters, subsequently preventing expression of Th2 cytokine genes and Th2 differentiation. Our results establish a novel role for Bcl11b in the regulatory loop critical for licensing the Th2 program in vivo.

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Mapping of Bcl11b binding in CD4+ T-cells during Th2 immune response

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Genome wide mapping of accessible chromatin in CD4+ T-cells during Th2 immune responses

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Transcriptome analysis of CD4+ T cells differentiated from wild-type and tumor bearing C57BL/6J mice

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Chromatin interaction analysis of transcription factors and NLRP3 in CD4+ T cells differentiated from wild-type and NLRP3KO mice

Project description:We report that the NLRP3 protein is able to interact with chromatin during Th2 differentiation

2015-05-12 | GSE64749 | GEO

Comparative analysis of the proteome of Th2 lymphocytes from WT or ASB2 KO mice

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