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10.1038/cmi.2017.9 http://scihub22266oqcxt.onion/10.1038/cmi.2017.9 C5423093!5423093!28366940     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Mol+Immunol 2017 ; 14 (5): 406-11 Nephropedia Template TP {{tp|p=28366940|t=2017. DOCK8 regulates signal transduction events to control immunity |pdf=|usr=}}{{28366940}} gab.com Text DOCK8 regulates signal transduction events to control immunity JO: Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28366940 #FOAvip Genetic mutations in the gene encoding DOCK8 cause an autosomal recessive form of hyper immunoglobulin E syndrome (AR-HIES), referred to as DOCK8 deficiency. DOCK8 deficiency in humans results in the onset of combined immunodeficiency disease (CID), clinically associated with chronic infections with diverse microbial pathogens, and a predisposition to malignancy. It is now becoming clear that DOCK8 regulates the function of diverse immune cell sub-types, particularly lymphocytes, to drive both innate and adaptive immune responses. Early studies demonstrated that DOCK8 is required for lymphocyte survival, migration and immune synapse formation, which translates to poor pathogen control in the absence of DOCK8. However, more recent advances have pointed to a crucial role for DOCK8 in regulating the signal transduction events that control transcriptional activity, cytokine production and functional polarization of immune cells. Here, we summarize recent advances in our understanding of DOCK8 function, paying particular attention to an emerging role as a signaling intermediate to promote immune responses to diverse external stimuli. Twit Text FOAVip DOCK8 regulates signal transduction events to control immunity ????Cell Mol Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28366940 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28366940 #FOAvip English Wikipedia <ref>{{Cite pmid|28366940}}</ref> DOCK8 regulates signal transduction events to control immunity #MMPMID28366940 Kearney CJ; Randall KL; Oliaro J Cell Mol Immunol 2017[May]; 14 (5): 406-11 PMID28366940show ga Genetic mutations in the gene encoding DOCK8 cause an autosomal recessive form of hyper immunoglobulin E syndrome (AR-HIES), referred to as DOCK8 deficiency. DOCK8 deficiency in humans results in the onset of combined immunodeficiency disease (CID), clinically associated with chronic infections with diverse microbial pathogens, and a predisposition to malignancy. It is now becoming clear that DOCK8 regulates the function of diverse immune cell sub-types, particularly lymphocytes, to drive both innate and adaptive immune responses. Early studies demonstrated that DOCK8 is required for lymphocyte survival, migration and immune synapse formation, which translates to poor pathogen control in the absence of DOCK8. However, more recent advances have pointed to a crucial role for DOCK8 in regulating the signal transduction events that control transcriptional activity, cytokine production and functional polarization of immune cells. Here, we summarize recent advances in our understanding of DOCK8 function, paying particular attention to an emerging role as a signaling intermediate to promote immune responses to diverse external stimuli. äDOCK8 regulates signal transduction events to control immunity (epmc).pdf DeepDyve Pubget Overpricing