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10.1016/j.immuni.2015.02.011 http://scihub22266oqcxt.onion/10.1016/j.immuni.2015.02.011 25786179!ä!25786179 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunity 2015 ; 42 (3): 566-79 Nephropedia Template TP {{tp|p=25786179|t=2015. Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection |pdf=|usr=}}{{25786179}} gab.com Text Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=25786179 #FOAvip Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK) cells, thus altering IL-33 responsiveness within the lung. Consequently, upon infection and release, increased local IL-33 significantly amplified type I proinflammatory responses via synergistic modulation of macrophage and NK cell function. Therefore, in COPD, smoke alters the lung microenvironment to facilitate an alternative IL-33-dependent exaggerated proinflammatory response to infection, exacerbating disease. Twit Text FOAVip Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=25786179 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25786179 #FOAvip English Wikipedia <ref>{{Cite pmid|25786179}}</ref> Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection #MMPMID25786179 Kearley J; Silver JS; Sanden C; Liu Z; Berlin AA; White N; Mori M; Pham TH; Ward CK; Criner GJ; Marchetti N; Mustelin T; Erjefalt JS; Kolbeck R; Humbles AA Immunity 2015[Mar]; 42 (3): 566-79 PMID25786179show ga Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK) cells, thus altering IL-33 responsiveness within the lung. Consequently, upon infection and release, increased local IL-33 significantly amplified type I proinflammatory responses via synergistic modulation of macrophage and NK cell function. Therefore, in COPD, smoke alters the lung microenvironment to facilitate an alternative IL-33-dependent exaggerated proinflammatory response to infection, exacerbating disease. |Animals[MESH] |Female[MESH] |Gene Expression Regulation[MESH] |Humans[MESH] |Immunity, Innate/*drug effects[MESH] |Influenza A virus/immunology[MESH] |Interleukin-1 Receptor-Like 1 Protein[MESH] |Interleukin-33[MESH] |Interleukins/deficiency/genetics/*immunology[MESH] |Killer Cells, Natural/immunology/pathology[MESH] |Lung/drug effects/immunology/pathology[MESH] |Lymphocytes/drug effects/immunology/pathology[MESH] |Macrophages/immunology/pathology[MESH] |Mice, Transgenic[MESH] |Nicotiana/chemistry[MESH] |Orthomyxoviridae Infections/etiology/genetics/*immunology/pathology[MESH] |Pulmonary Disease, Chronic Obstructive/genetics/*immunology/pathology[MESH] |Receptors, Interleukin/deficiency/genetics/*immunology[MESH] |Respiratory Mucosa/drug effects/immunology/pathology[MESH] |Signal Transduction[MESH] |Smoke/*adverse effects[MESH]Cigarette smoke silences innate lymphoid cell function and facilitates(epmc).pdf DeepDyve Pubget Overpricing