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10.1089/jir.2015.0072 http://scihub22266oqcxt.onion/10.1089/jir.2015.0072 26308503!ä!26308503 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Interferon+Cytokine+Res 2015 ; 35 (12): 925-34 Nephropedia Template TP {{tp|p=26308503|t=2015. The Role of Virus Infection in Deregulating the Cytokine Response to Secondary Bacterial Infection |pdf=|usr=}}{{26308503}} gab.com Text The Role of Virus Infection in Deregulating the Cytokine Response to Secondary Bacterial Infection JO: J Interferon Cytokine Res http://www.kidney.de/pget.php?&tw=1&pmid=26308503 #FOAvip Proinflammatory cytokines are produced by macrophages and dendritic cells (DCs) after infection to stimulate T helper (Th) cells, linking innate and adaptive immunity. Virus infections can deregulate the proinflammatory cytokine response like tumor necrosis factor-alpha and interleukin (IL)-2, making the host more susceptible to secondary bacterial infections. Studies using various viruses such as lymphocytic choriomeningitis virus, influenza A virus, and human immunodeficiency virus have revealed several intriguing mechanisms that account for the increased susceptibility to several prevalent bacterial infections. In particular, type I interferons induced during a virus infection have been observed to play a role in suppressing the production of some key antibacterial proinflammatory cytokines such as IL-23 and IL-17. Other suppressive mechanisms as a result of cytokine deregulation by viral infections include reduced function of immune cells such as DC, macrophage, natural killer, CD4(+), and CD8(+) T cells leading to impaired clearance of secondary bacterial infections. In this study, we highlight some of the immune mechanisms that become deregulated by viral infections, and can thus become defective during secondary bacterial infections. Twit Text FOAVip The Role of Virus Infection in Deregulating the Cytokine Response to Secondary Bacterial Infection ????J Interferon Cytokine Res http://www.kidney.de/pget.php?&tw=1&pmid=26308503 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26308503 #FOAvip English Wikipedia <ref>{{Cite pmid|26308503}}</ref> The Role of Virus Infection in Deregulating the Cytokine Response to Secondary Bacterial Infection #MMPMID26308503 Mehta D; Petes C; Gee K; Basta S J Interferon Cytokine Res 2015[Dec]; 35 (12): 925-34 PMID26308503show ga Proinflammatory cytokines are produced by macrophages and dendritic cells (DCs) after infection to stimulate T helper (Th) cells, linking innate and adaptive immunity. Virus infections can deregulate the proinflammatory cytokine response like tumor necrosis factor-alpha and interleukin (IL)-2, making the host more susceptible to secondary bacterial infections. Studies using various viruses such as lymphocytic choriomeningitis virus, influenza A virus, and human immunodeficiency virus have revealed several intriguing mechanisms that account for the increased susceptibility to several prevalent bacterial infections. In particular, type I interferons induced during a virus infection have been observed to play a role in suppressing the production of some key antibacterial proinflammatory cytokines such as IL-23 and IL-17. Other suppressive mechanisms as a result of cytokine deregulation by viral infections include reduced function of immune cells such as DC, macrophage, natural killer, CD4(+), and CD8(+) T cells leading to impaired clearance of secondary bacterial infections. In this study, we highlight some of the immune mechanisms that become deregulated by viral infections, and can thus become defective during secondary bacterial infections. |*Coinfection[MESH] |*Host-Pathogen Interactions/immunology[MESH] |Animals[MESH] |Bacterial Infections/*immunology/*metabolism/microbiology[MESH] |Cytokines/*metabolism[MESH] |Disease Models, Animal[MESH] |Humans[MESH] |Immunomodulation[MESH] |Inflammation Mediators/metabolism[MESH] |Interferon Type I/metabolism[MESH] |Lymphocytic choriomeningitis virus/immunology[MESH] |T-Lymphocyte Subsets/immunology/metabolism[MESH]The Role of Virus Infection in Deregulating the Cytokine Response to S(epmc).pdf DeepDyve Pubget Overpricing