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STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation
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STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation
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Journal Article
STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation
2014
Overview
T helper （Tn）-cell subsets, such as TH1 and TH17, mediate inflammation in both peripheral tissues and central nervous system. Here we show that STAT5 is required for T helper-cell pathogenicity in autoimmune neuroinflammation but not in experimental colitis. Although STAT5 promotes regulatory T cell generation and immune suppression, loss of STAT5 in CD4~ T cells resulted in diminished development of experimental autoimmune encephalomyelitis （EAE）, a mouse model of multiple sclerosis. Our results showed that loss of encephalitogenic activity of STAT5-deficient autoreaetive CD4＋ T cells was independent of IFN-7 or interleukin 17 （IL-17） production, but was due to the impaired expression of granulocyte-macrophage colony-stimulating factor （GM-CSF）, a crucial mediator of T-cell pathogenicity. We further showed that IL-7-activated STAT5 promotes the generation of GM-CSF-producing CD4＋ T cells, which were preferentially able to induce more severe EAE than TH17 or TH1 cells. Consistent with GM-CSF-produc- ing cells being a distinct subset of TH cells, the differentiation program of these cells was distinct from that of TH17 or TH1 cells. We further found that IL-3 was secreted in a similar pattern as GM-CSF in this subset of T, cells. In conclusion, the IL-7-STAT5 axis promotes the generation of GM-CSF/IL-3-producing T, cells. These cells display a distinct transcriptional profile and may represent a novel subset of T helper cells which we designate as TH-GM.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Biomedical and Life Sciences
/ Encephalomyelitis, Autoimmune, Experimental - genetics
/ Encephalomyelitis, Autoimmune, Experimental - immunology
/ Encephalomyelitis, Autoimmune, Experimental - pathology
/ GM-CSF
/ Granulocyte-Macrophage Colony-Stimulating Factor - analysis
/ Granulocyte-Macrophage Colony-Stimulating Factor - immunology
/ Mice
/ Original
/ STAT5
/ STAT5 Transcription Factor - analysis
/ STAT5 Transcription Factor - genetics
/ STAT5 Transcription Factor - immunology
/ T-Lymphocytes, Helper-Inducer - immunology
/ T-Lymphocytes, Helper-Inducer - metabolism
/ T-Lymphocytes, Helper-Inducer - pathology
/ 中枢神经系统
/ 子集
/ 炎症
/ 自身免疫性
/ 调节性T细胞
