The contribution of transcription factor IRF1 to the interferon-big gamma-interleukin 12 signaling axis and TH1 versus TH-17 differentiation of CD4+ T cells

Interleukin-12 and IFN-γ usually power T helper cell type 1 differentiation. The IFN-γ-induced transcription factor IRF1 seems to be essential in T helper cell type 1 differentiation by acting on IL-12rb1, the gene encoding for the beta1 subunit of the Interleukin-12 receptor (IL-12Rbeta1). This was reported by Shin-ichi Kano and collaborators from the University of Tokyo. According to their research, IRF1 interacts directly with the IL-12rb1 promoter in CD4+ T cells and activates it.

Recent evidence reveals that the IRF1-dependent initiation of IL-12Rbeta1 was crucial for IFN-γ-Interleukin-12 signalling. It was not required for Interleukin-23-Interleukin-17 signalling. Since Interleukin-12 as well as Interleukin-23 bind and transmit signals through IL-12Rbeta1, the scientists propose that clear thresholds of IL-12Rbeta1 expression are essential for T helper cell type 1 versus T helper cell type 17 differentiation.

Related antibodies on antibodies-online.com:

Interleukin 12 (IL-12)

Interleukin 12 Receptor beta-1

Interferon-γ (IFN-γ)

T cells

CD4+ T cells

IRF1

Interleukin 23 (IL-23)

Interleukin 17 (IL-17)

Interleukin 12/23 (p40)

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Antibodies for the research area transcription factors: »Show antibodies