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We are analyzing https://www.nature.com/articles/ni.2031.

Title:
The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF | Nature Immunology
Description:
The development of experimental autoimmune encephalomyelitis has been attributed to cells of the TH1 or TH17 subset of helper T cells. Becher and Rostami and their colleagues show that IL-23-induced production of the cytokine GM-CSF underlies disease development and severity. Interleukin 17 (IL-17)-producing helper T cells (TH17 cells) require exposure to IL-23 to become encephalitogenic, but the mechanism by which IL-23 promotes their pathogenicity is not known. Here we found that IL-23 induced production of the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) in TH17 cells and that GM-CSF had an essential role in their encephalitogenicity. Our findings identify a chief mechanism that underlies the important role of IL-23 in autoimmune diseases. IL-23 induced a positive feedback loop whereby GM-CSF secreted by TH17 cells stimulated the production of IL-23 by antigen-presenting cells. Such cross-regulation of IL-23 and GM-CSF explains the similar pattern of resistance to autoimmunity when either of the two cytokines is absent and identifies TH17 cells as a crucial source of GM-CSF in autoimmune inflammation.
Website Age:
30 years and 10 months (reg. 1994-08-11).

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Keywords {πŸ”}

pubmed, article, cas, google, scholar, cells, nature, immunol, autoimmune, central, gmcsf, production, access, content, cytokine, ilproducing, encephalomyelitis, interleukin, development, cell, nat, receptor, essential, cookies, immunology, helper, differentiation, inflammatory, privacy, elbehi, ciric, factor, inflammation, experimental, exp, med, data, information, journal, encephalitogenicity, rostami, colonystimulating, autoimmunity, pathogenic, regulatory, sci, usa, lineage, mice, required,

Topics {βœ’οΈ}

nature portfolio permissions reprints privacy policy granulocyte-macrophage colony-stimulating factor advertising il-1/il-1r antagonist system social media data protection nature 441 nature 448 nature 421 nature 467 nature article el-behi guang-xian zhang author correspondence central nervous system personal data th17-driven inflammatory disease 17 cell-mediated pathology experimental autoimmune encephalomyelitis springerlink instant access gm-csf mediates autoimmunity permissions anti-gm-csf ameliorates autoimmune encephalomyelitis microbial lipopeptides induce adult mouse microglia cytokine gm-csf reciprocal developmental pathways il-9 induces differentiation peripherally derived monocytes transcription factor activities privacy gm-csf explains autoimmune neuro-inflammation cell surface receptor competing financial interests gm-csf production gm-csf secreted interleukin-6 mrna induced pathogenic th17 cells il-23-induced production il-23 induced production abdolmohamad rostami il-23-dependent fashion il-17-producing cells pathogenic effector th17 t-bet regulates autoimmune diseases

Schema {πŸ—ΊοΈ}

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