Interferon gamma-induction of TH1-like regulatory T cells controls anti-viral responses
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA925222 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23116572_1.fastq.gz | Fastqsanger.gz | |||
| SRR23116572_2.fastq.gz | Fastqsanger.gz | |||
| SRR23116573_1.fastq.gz | Fastqsanger.gz | |||
| SRR23116573_2.fastq.gz | Fastqsanger.gz | |||
| SRR23116574.fastq.gz | Fastqsanger.gz |
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Project description:Type 1 T helper (Th1) cells play a critical role in host defense against intracellular pathogens and in autoimmune diseases by producing a key inflammatory cytokine interferon (IFN)-γ; some Th1 cells can also be anti-inflammatory through producing IL-10. However, the molecular switch for regulating the differentiation of inflammatory and anti-inflammatory Th1 cells is still elusive. Here we show that Bhlhe40-deficient CD4 Th1 cells produced less IFN-γ but substantially more IL-10 than wild type Th1 cells. Bhlhe40-mediated IFN-γ production was independent of transcription factor T-bet regulation. Mice with conditional deletion of Bhlhe40 in T cells succumbed to Toxoplasma gondii infection and blockage of IL-10 signaling during infection rescued these mice from death. Thus, our results demonstrate that transcription factor Bhlhe40 is a molecular switch for determining the fate of inflammatory and anti-inflammatory Th1 cells.
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