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10.1038/s41467-017-01771-2

http://scihub22266oqcxt.onion/10.1038/s41467-017-01771-2
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C5688161!5688161!29142230
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suck abstract from ncbi


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pmid29142230      Nat+Commun 2017 ; 8 (ä): ä
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  • Unique transcriptome signatures and GM-CSF expression in lymphocytes from patients with spondyloarthritis #MMPMID29142230
  • Al-Mossawi MH; Chen L; Fang H; Ridley A; de Wit J; Yager N; Hammitzsch A; Pulyakhina I; Fairfax BP; Simone D; Yi Y; Bandyopadhyay S; Doig K; Gundle R; Kendrick B; Powrie F; Knight JC; Bowness P
  • Nat Commun 2017[]; 8 (ä): ä PMID29142230show ga
  • Spondyloarthritis encompasses a group of common inflammatory diseases thought to be driven by IL-17A-secreting type-17 lymphocytes. Here we show increased numbers of GM-CSF-producing CD4 and CD8 lymphocytes in the blood and joints of patients with spondyloarthritis, and increased numbers of IL-17A+GM-CSF+ double-producing CD4, CD8, ?? and NK cells. GM-CSF production in CD4 T cells occurs both independently and in combination with classical Th1 and Th17 cytokines. Type 3 innate lymphoid cells producing predominantly GM-CSF are expanded in synovial tissues from patients with spondyloarthritis. GM-CSF+CD4+ cells, isolated using a triple cytokine capture approach, have a specific transcriptional signature. Both GM-CSF+ and IL-17A+GM-CSF+ double-producing CD4 T cells express increased levels of GPR65, a proton-sensing receptor associated with spondyloarthritis in genome-wide association studies and pathogenicity in murine inflammatory disease models. Silencing GPR65 in primary CD4 T cells reduces GM-CSF production. GM-CSF and GPR65 may thus serve as targets for therapeutic intervention of spondyloarthritis.
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