Cytokine receptor modulation by interleukin-2 broadly regulates T helper cell lineage differentiation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA137397 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR098982.fastq.gz | Fastqsanger.gz | |||
| SRR098983.fastq.gz | Fastqsanger.gz | |||
| SRR098984.fastq.gz | Fastqsanger.gz | |||
| SRR098985.fastq.gz | Fastqsanger.gz | |||
| SRR098986.fastq.gz | Fastqsanger.gz |
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Project description:T helper (Th) cells control host defense to pathogens. IL 12R expression is required for Th1, IL-4Rα for Th2, and IL-6Rα/gp130 for Th17 differentiation to allow responsiveness to IL-12, IL-4, and IL-6, respectively. IL-2 via STAT5 controls Th2 differentiation by regulating the Th2 cytokine gene cluster and Il4ra expression. Here we show that IL-2 regulates Th1 differentiation, inducing STAT5-dependent IL-12Rβ2 and T-bet expression, with impaired human Th1 differentiation when IL-2 was blocked. Th1 differentiation was also impaired in mouse Il2-/- T cells but restored by IL-12Rβ2 expression. Consistent with IL-2’s inhibition of Th17 differentiation, IL-2 decreased Il6ra and Il6st/gp130 expression, and Il6st augmented Th17 differentiation even when IL-2 was present. Thus, IL-2 influences T-cell differentiation by modulating cytokine receptor expression to help specify/maintain differentiated states.
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