IFN-γ represses IL-4 expression via IRF-1 and IRF-2
Polarization of CD4+ T helper cells toward either a Th1 or Th2 response can significantly influence host immunity to pathogens. IL-4 and IFN-γ are the signature cytokines of Th2 and Th1 cells, respectively. IFN-γ was shown to assist Th1 development by promoting IL-12 and IL-12 receptor expression. S...
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| Main Authors: | , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
16 December 2002
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| In: |
Immunity
Year: 2002, Volume: 17, Issue: 6, Pages: 703-712 |
| ISSN: | 1097-4180 |
| DOI: | 10.1016/S1074-7613(02)00471-5 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/S1074-7613(02)00471-5 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S1074761302004715 |
| Author Notes: | Bernd Elser, Michael Lohoff, Sonja Kock, Marco Giaisi, Sabine Kirchhoff, Peter H. Krammer, and Min Li-Weber |
MARC
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| 520 | |a Polarization of CD4+ T helper cells toward either a Th1 or Th2 response can significantly influence host immunity to pathogens. IL-4 and IFN-γ are the signature cytokines of Th2 and Th1 cells, respectively. IFN-γ was shown to assist Th1 development by promoting IL-12 and IL-12 receptor expression. So far, direct influence of Th2 cytokine expression by IFN-γ has not been described. We show here that IFN-γ directly suppresses IL-4 gene expression. IRF-1 and IRF-2 induced by IFN-γ bind to three distinct IL-4 promoter sites and function as transcriptional repressors. Our data demonstrate a direct negative feedback of IFN-γ on expression of the Th2 cytokine gene IL-4 and, thus, provide evidence for another important mechanism by which IFNγ assists Th1 and attenuates Th2 responses. | ||
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