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10.1016/j.imbio.2004.04.002 http://scihub22266oqcxt.onion/10.1016/j.imbio.2004.04.002 15481135!ä!15481135 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunobiology 2004 ; 209 (1-2): 3-10 Nephropedia Template TP {{tp|p=15481135|t=2004. CD14 is required for influenza A virus-induced cytokine and chemokine production |pdf=|usr=}}{{15481135}} gab.com Text CD14 is required for influenza A virus-induced cytokine and chemokine production JO: Immunobiology http://www.kidney.de/pget.php?&tw=1&pmid=15481135 #FOAvip Infection of monocytes and macrophages by influenza A virus leads to proinflammatory and chemotactic cytokine production. The signalling pathways linking innate immune virus recognition to cytokine expression are little understood. Here, we report that blocking of CD14 on human monocytes by specific antibody or use of CD14-deficient murine macrophages abolished influenza A virus-induced cytokine production. Toll-like receptor (TLR) 2 and 4-deficient murine macrophages remained fully responsive. These results suggest that CD14, together with a TLR other than TLR2 or 4, is an essential coreceptor of the influenza A virus sensing recognition system. Twit Text FOAVip CD14 is required for influenza A virus-induced cytokine and chemokine production ????Immunobiology http://www.kidney.de/pget.php?&tw=1&pmid=15481135 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15481135 #FOAvip English Wikipedia <ref>{{Cite pmid|15481135}}</ref> CD14 is required for influenza A virus-induced cytokine and chemokine production #MMPMID15481135 Pauligk C; Nain M; Reiling N; Gemsa D; Kaufmann A Immunobiology 2004[]; 209 (1-2): 3-10 PMID15481135show ga Infection of monocytes and macrophages by influenza A virus leads to proinflammatory and chemotactic cytokine production. The signalling pathways linking innate immune virus recognition to cytokine expression are little understood. Here, we report that blocking of CD14 on human monocytes by specific antibody or use of CD14-deficient murine macrophages abolished influenza A virus-induced cytokine production. Toll-like receptor (TLR) 2 and 4-deficient murine macrophages remained fully responsive. These results suggest that CD14, together with a TLR other than TLR2 or 4, is an essential coreceptor of the influenza A virus sensing recognition system. |Animals[MESH] |Cells, Cultured[MESH] |Chemokines/*metabolism[MESH] |Cytokines/*metabolism[MESH] |Humans[MESH] |Influenza A virus/*immunology[MESH] |Lipopolysaccharide Receptors/*metabolism[MESH] |Macrophages/metabolism[MESH] |Membrane Glycoproteins/*metabolism[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |Monocytes/metabolism[MESH] |Receptors, Cell Surface/*metabolism[MESH] |Toll-Like Receptor 2[MESH]CD14 is required for influenza A virus-induced cytokine and chemokine (epmc).pdf DeepDyve Pubget Overpricing