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10.1038/s41598-017-04260-0

http://scihub22266oqcxt.onion/10.1038/s41598-017-04260-0
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C5478593!5478593!28634408
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suck abstract from ncbi


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pmid28634408      Sci+Rep 2017 ; 7 (ä): ä
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  • A tightly regulated IL-22 response maintains immune functions and homeostasis in systemic viral infection #MMPMID28634408
  • Yi P; Liang Y; Yuan DMK; Jie Z; Kwota Z; Chen Y; Cong Y; Fan X; Sun J
  • Sci Rep 2017[]; 7 (ä): ä PMID28634408show ga
  • Interleukin-22 (IL-22) plays an important role in host immunity and tissue homeostasis in infectious and inflammatory diseases. However, the function and regulation of IL-22 in viral infection remain largely unknown. Here, we report that viral infection triggered early IL-22 production from the liver and lymphoid organs. ?? T cells are the main immune cells to produce IL-22 in the liver, a process mediated by the IL-23/phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin complex 1 (mTORC1) signaling pathway. In the presence of IL-23, IL-22 production is independent of aryl hydrocarbon receptor (AhR) signaling. In acute and persistent viral infections, IL-22 deficiency resulted in thymic and splenic hypertrophy, while excessive IL-22 induced atrophy in these lymphoid organs. Moreover, IL-22 deficiency enhanced T cell responses to promote viral clearance, but increased IL-22 in vivo decreased T cell numbers and functions in the liver and lymphoid tissues. Together, our findings reveal a significant effect of the IL-23/PI3K/mTORC1 axis on regulating IL-22 production and also identify a novel role of IL-22 in controlling antiviral T cell responses in the non-lymphoid and lymphoid organs during acute and persistent viral infections.
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