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10.1165/rcmb.2014-0448OC

http://scihub22266oqcxt.onion/10.1165/rcmb.2014-0448OC
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C4742936!4742936!25923039
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suck abstract from ncbi


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pmid25923039      Am+J+Respir+Cell+Mol+Biol 2015 ; 53 (6): 822-33
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  • Regulation of Retinoic Acid Receptor Beta by Interleukin-15 in the Lung during Cigarette Smoking and Influenza Virus Infection #MMPMID25923039
  • Wang J; Liu W; Marion C; Singh R; Andrews N; Lee CG; Elias JA; Dela Cruz CS
  • Am J Respir Cell Mol Biol 2015[Dec]; 53 (6): 822-33 PMID25923039show ga
  • Virus-induced exacerbations often lead to further impairment of lung function in chronic obstructive pulmonary disease. IL-15 is critical in antiviral immune responses. Retinoic acid (RA) signaling plays an important role in tissue maintenance and repair, particularly in the lung. We studied RA signaling and its relation to IL-15 in the lung during cigarette smoke (CS) exposure and influenza virus infection. In vivo studies show that RA signaling is diminished by long-term CS exposure or influenza virus infection alone, which is further attenuated during infection after CS exposure. RA receptor ? (RAR?) is specifically decreased in the lung of IL-15 transgenic (overexpression; IL-15Tg) mice, and a greater reduction in RAR? is found in these mice compared with wild-type (WT) mice after infection. RAR? is increased in IL-15 knockout (IL-15KO) mice compared with WT mice after infection, and the additive effect of CS and virus on RAR? down-regulation is diminished in IL-15KO mice. IL-15 receptor ? (IL-15R?) is increased and RAR? is significantly decreased in lung interstitial macrophages from IL-15Tg mice compared with WT mice. In vitro studies show that IL-15 down-regulates RAR? in macrophages via IL-15R? signaling during influenza virus infection. These studies suggest that RA signaling is significantly diminished in the lung by CS exposure and influenza virus infection. IL-15 specifically down-regulates RAR? expression, and RAR? may play a protective role in lung injury caused by CS exposure and viral infections.
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