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10.3389/fimmu.2017.01403

http://scihub22266oqcxt.onion/10.3389/fimmu.2017.01403
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C5666299!5666299!29163483
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suck abstract from ncbi


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pmid29163483      Front+Immunol 2017 ; 8 (ä): ä
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  • CD4 T-Cell Dysregulation in Psoriatic Arthritis Reveals a Regulatory Role for IL-22 #MMPMID29163483
  • Ezeonyeji A; Baldwin H; Vukmanovic-Stejic M; Ehrenstein MR
  • Front Immunol 2017[]; 8 (ä): ä PMID29163483show ga
  • Dysregulation of interleukin-22 (IL-22) has been associated with autoimmune diseases but divergent effects upon inflammation have hampered efforts to define its contribution to pathogenesis. Here, we examined the role of IL-22 in patients with psoriatic arthritis (PsA). In the peripheral blood of PsA patients, there was a decrease in IL-22+CD4+ T cells compared with healthy controls resulting in a heightened CD4+ IFN?+/IL-22+ ratio accompanied by diminished CCR6 expression. IL-22 expressing cells were depleted primarily from the central memory CD4 T-cell subset in PsA patients. Paradoxically IL-22 and particularly interferon-gamma (IFN?) production were elevated within a CD4+ T-cell subset with phenotypic markers characteristic of naïve T cells (CD3+CD4+CD27+CD45RA+CCR7+CD95?IL-2R??) from PsA patients with the highest IFN?+/IL-22+ ratio of all the CD4 subsets. These unconventional ?naïve? CD4+ T cells from PsA patients displayed some phenotypic and functional characteristics of memory cells including a marked proliferative response. Increased IFN? production from these unconventional ?naïve? T cells from PsA patients promoted greater expression of the chemo-attractant CXCL9 by HaCaT keratinocytes compared with their healthy counterparts. Treatment with anti-TNF therapy reversed these abnormalities in this T-cell subset though did not affect the frequency of IL-22+ T cells overall. Furthermore, blockade of IL-22 enhanced the IFN? mediated release of CXCL-9. These results reveal CD4+ T-cell dysregulation in patients with PsA which can be reversed by anti-TNF and highlight the regulatory properties of IL-22 with important implications for therapeutic approaches that inhibit its production.
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