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10.1002/eji.201242683 http://scihub22266oqcxt.onion/10.1002/eji.201242683 23255009!3752658!23255009     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23255009&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Eur+J+Immunol 2012 ; 42 (12): 3126-35 Nephropedia Template TP {{tp|p=23255009|t=2012. Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans |pdf=|usr=}}{{23255009}} gab.com Text Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans JO: Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23255009 #FOAvip Most Toll-like-receptors (TLRs) and interleukin-1 receptors (IL-1Rs) signal via myeloid differentiation primary response 88 (MyD88) and interleukin-1 receptor-associated kinase 4 (IRAK-4). The combined roles of these two receptor families in the course of experimental infections have been assessed in MyD88- and IRAK-4-deficient mice for almost fifteen years. These animals have been shown to be susceptible to 46 pathogens: 27 bacteria, eight viruses, seven parasites, and four fungi. Humans with inborn MyD88 or IRAK-4 deficiency were first identified in 2003. They suffer from naturally occurring life-threatening infections caused by a small number of bacterial species, although the incidence and severity of these infections decrease with age. Mouse TLR- and IL-1R-dependent immunity mediated by MyD88 and IRAK-4 seems to be vital to combat a wide array of experimentally administered pathogens at most ages. By contrast, human TLR- and IL-1R-dependent immunity mediated by MyD88 and IRAK-4 seems to be effective in the natural setting against only a few bacteria and is most important in infancy and early childhood. The roles of TLRs and IL-1Rs in protective immunity deduced from studies in mutant mice subjected to experimental infections should therefore be reconsidered in the light of findings for natural infections in humans carrying mutations as discussed in this review. Twit Text FOAVip Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans ????Eur J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23255009 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23255009 #FOAvip English Wikipedia <ref>{{Cite pmid|23255009}}</ref> Experimental and natural infections in MyD88- and IRAK-4-deficient mice and humans #MMPMID23255009 von Bernuth H; Picard C; Puel A; Casanova JL Eur J Immunol 2012[Dec]; 42 (12): 3126-35 PMID23255009show ga Most Toll-like-receptors (TLRs) and interleukin-1 receptors (IL-1Rs) signal via myeloid differentiation primary response 88 (MyD88) and interleukin-1 receptor-associated kinase 4 (IRAK-4). The combined roles of these two receptor families in the course of experimental infections have been assessed in MyD88- and IRAK-4-deficient mice for almost fifteen years. These animals have been shown to be susceptible to 46 pathogens: 27 bacteria, eight viruses, seven parasites, and four fungi. Humans with inborn MyD88 or IRAK-4 deficiency were first identified in 2003. They suffer from naturally occurring life-threatening infections caused by a small number of bacterial species, although the incidence and severity of these infections decrease with age. Mouse TLR- and IL-1R-dependent immunity mediated by MyD88 and IRAK-4 seems to be vital to combat a wide array of experimentally administered pathogens at most ages. By contrast, human TLR- and IL-1R-dependent immunity mediated by MyD88 and IRAK-4 seems to be effective in the natural setting against only a few bacteria and is most important in infancy and early childhood. The roles of TLRs and IL-1Rs in protective immunity deduced from studies in mutant mice subjected to experimental infections should therefore be reconsidered in the light of findings for natural infections in humans carrying mutations as discussed in this review. |Animals[MESH] |Bacterial Infections/genetics/*immunology[MESH] |Disease Models, Animal[MESH] |Humans[MESH] |Immunologic Deficiency Syndromes/genetics/*immunology[MESH] |Interleukin-1 Receptor-Associated Kinases/genetics/*immunology[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Myeloid Differentiation Factor 88/genetics/*immunology[MESH] |Primary Immunodeficiency Diseases[MESH] |Receptors, Interleukin-1/genetics/immunology[MESH]Experimental and natural infections in MyD88- and IRAK-4-deficient mic(epmc).pdf DeepDyve Pubget Overpricing