In differentiated CD4+ T Cells, interleukin 4 production is cytokine-autonomous, whereas interferon γ production iscytokine-dependent

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CD4+T cells from T cell receptor transgenic mice that have been vigorously primed to be interleukin (IL)-4 producers (TH2cells) are capable of producing IL-4 even if restimulated in the absence of IL-4 and in the presence of IL-12. T cells vigorously primed in the absence of IL-4 (TH1cells) fail to produce IL-4 even if restimulated under conditions that would cause a naive T cell to produce IL-4. In contrast, interferon γ (IFN-γ ) production is highly cytokine-regulated. T cells primed in the presence of IL-4 develop into IFN-γ producers if IFN-γ is included in the priming culture and if the cells are challenged in the presence of IL-12, presumably reflecting the role of IFN-γ in inducing responsiveness to IL-12. Cells primed in the absence of IL-4 become highly responsive to IL-12 if IFN-γ is included in the priming culture, and these cells are excellent IFN-γ producers upon challenge; IL-12 considerably enhances their production of IFN-γ . If cells are primed in the absence of IL-4 and IFN-γ , they show very weak responsiveness to IL-12 as determined by STAT-4 activation. However, these cells acquire IL-12 responsiveness if cultured with IFN-γ for a period as short as 4 hr. Thereafter, they produce large amounts of IFN-γ upon challenge with antigen in the presence of IL-12. These results indicate that in primed CD4+T cells, IL-4 production is largely cytokine-autonomous, whereas IFN-γ production is highly cytokine-regulated.

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Tyrosine phosphorylation Monoclonal-antibodies Receptor Th1 Transcription Invitro Clones T(h)1 Assay Stat4