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10.1038/s41385-020-0280-z http://scihub22266oqcxt.onion/10.1038/s41385-020-0280-z 32152414!7483155!32152414     free     free     free 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 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mucosal+Immunol 2021 ; 14 (1): 209-218 Nephropedia Template TP {{tp|p=32152414|t=2021. NMP4 regulates the innate immune response to influenza A virus infection |pdf=|usr=}}{{32152414}} gab.com Text NMP4 regulates the innate immune response to influenza A virus infection JO: Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32152414 #FOAvip Severe influenza A virus infection typically triggers excessive and detrimental lung inflammation with massive cell infiltration and hyper-production of cytokines and chemokines. We identified a novel function for nuclear matrix protein 4 (NMP4), a zinc-finger-containing transcription factor playing roles in bone formation and spermatogenesis, in regulating antiviral immune response and immunopathology. Nmp4-deficient mice are protected from H1N1 influenza infection, losing only 5% body weight compared to a 20% weight loss in wild type mice. While having no effects on viral clearance or CD8/CD4 T cell or humoral responses, deficiency of Nmp4 in either lung structural cells or hematopoietic cells significantly reduces the recruitment of monocytes and neutrophils to the lungs. Consistent with fewer innate cells in the airways, influenza-infected Nmp4-deficient mice have significantly decreased expression of chemokine genes Ccl2, Ccl7 and Cxcl1 as well as pro-inflammatory cytokine genes Il1b and Il6. Furthermore, NMP4 binds to the promoters and/or conserved non-coding sequences of the chemokine genes and regulates their expression in mouse lung epithelial cells and macrophages. Our data suggest that NMP4 functions to promote monocyte- and neutrophil-attracting chemokine expression upon influenza A infection, resulting in exaggerated innate inflammation and lung tissue damage. Twit Text FOAVip NMP4 regulates the innate immune response to influenza A virus infection ????Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32152414 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32152414 #FOAvip English Wikipedia <ref>{{Cite pmid|32152414}}</ref> NMP4 regulates the innate immune response to influenza A virus infection #MMPMID32152414 Yang S; Adaway M; Du J; Huang S; Sun J; Bidwell JP; Zhou B Mucosal Immunol 2021[Jan]; 14 (1): 209-218 PMID32152414show ga Severe influenza A virus infection typically triggers excessive and detrimental lung inflammation with massive cell infiltration and hyper-production of cytokines and chemokines. We identified a novel function for nuclear matrix protein 4 (NMP4), a zinc-finger-containing transcription factor playing roles in bone formation and spermatogenesis, in regulating antiviral immune response and immunopathology. Nmp4-deficient mice are protected from H1N1 influenza infection, losing only 5% body weight compared to a 20% weight loss in wild type mice. While having no effects on viral clearance or CD8/CD4 T cell or humoral responses, deficiency of Nmp4 in either lung structural cells or hematopoietic cells significantly reduces the recruitment of monocytes and neutrophils to the lungs. Consistent with fewer innate cells in the airways, influenza-infected Nmp4-deficient mice have significantly decreased expression of chemokine genes Ccl2, Ccl7 and Cxcl1 as well as pro-inflammatory cytokine genes Il1b and Il6. Furthermore, NMP4 binds to the promoters and/or conserved non-coding sequences of the chemokine genes and regulates their expression in mouse lung epithelial cells and macrophages. Our data suggest that NMP4 functions to promote monocyte- and neutrophil-attracting chemokine expression upon influenza A infection, resulting in exaggerated innate inflammation and lung tissue damage. |*Immunity, Innate[MESH] |*Immunomodulation/genetics[MESH] |Adaptive Immunity[MESH] |Animals[MESH] |Chemotaxis, Leukocyte/genetics/immunology[MESH] |Cytokines/metabolism[MESH] |Disease Models, Animal[MESH] |Disease Susceptibility[MESH] |Host-Pathogen Interactions/immunology[MESH] |Inflammation Mediators/metabolism[MESH] |Influenza A virus/*immunology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Monocytes/immunology/metabolism/pathology[MESH] |Neutrophils/immunology/metabolism/pathology[MESH] |Nuclear Matrix-Associated Proteins/*genetics/metabolism[MESH] |Orthomyxoviridae Infections/*genetics/*immunology/metabolism/virology[MESH]NMP4 regulates the innate immune response to influenza A virus infecti(epmc).pdf DeepDyve Pubget Overpricing