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10.1016/j.jaci.2016.04.023 http://scihub22266oqcxt.onion/10.1016/j.jaci.2016.04.023 C5099100!5099100 !27350570     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27350570 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Allergy+Clin+Immunol 2016 ; 138 (5 ): 1384-1394.e2 Nephropedia Template TP {{tp|p=27350570 |t=2016. Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes T(H)17 cell differentiation |pdf=|usr=}}{{27350570 }} gab.com Text Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes T(H)17 cell differentiation JO: J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27350570 #FOAvip BACKGROUND: The autosomal recessive hyper-IgE syndrome (HIES) caused by dedicator of cytokinesis 8 (DOCK8) deficiency shares clinical features with autosomal dominant HIES because of signal transducer and activator of transcription 3 (STAT3) mutations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of T(H)17 cell dysfunction. The mechanisms underlying this phenotypic overlap are unclear. OBJECTIVE: We sought to elucidate common mechanisms operating in the different forms of HIES. METHODS: We analyzed the differentiation of CD4(+) T(H) cell subsets in control and DOCK8-deficient subjects. We also examined the role of DOCK8 in regulating STAT3 activation in T cells. T(H) cell differentiation was analyzed by ELISA, flow cytometry, and real-time PCR measurements of cytokines and T(H) cell transcription factors. The interaction of DOCK8 and STAT3 signaling pathways was examined by using flow cytometry, immunofluorescence, coimmunoprecipitation, and gene expression analysis. RESULTS: There was a profound block in the differentiation of DOCK8-deficient naive CD4(+) T cells into T(H)17 cells. A missense mutation that disrupts DOCK8 guanine nucleotide exchange factor (GEF) activity while sparing protein expression also impaired T(H)17 cell differentiation. DOCK8 constitutively associated with STAT3 independent of GEF activity, whereas it regulated STAT3 phosphorylation in a GEF activity-dependent manner. DOCK8 also promoted STAT3 translocation to the nucleus and induction of STAT3-dependent gene expression. CONCLUSION: DOCK8 interacts with STAT3 and regulates its activation and the outcome of STAT3-dependent T(H)17 differentiation. These findings might explain the phenotypic overlap between DOCK8 deficiency and autosomal dominant HIES. Twit Text FOAVip Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes T(H)17 cell differentiation ????J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27350570 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27350570 #FOAvip English Wikipedia <ref>{{Cite pmid|27350570 }}</ref> Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes T(H)17 cell differentiation #MMPMID27350570 Keles S ; Charbonnier LM ; Kabaleeswaran V ; Reisli I ; Genel F ; Gulez N ; Al-Herz W ; Ramesh N ; Perez-Atayde A ; Karaca NE ; Kutukculer N ; Wu H ; Geha RS ; Chatila TA J Allergy Clin Immunol 2016[Nov]; 138 (5 ): 1384-1394.e2 PMID27350570 show ga BACKGROUND: The autosomal recessive hyper-IgE syndrome (HIES) caused by dedicator of cytokinesis 8 (DOCK8) deficiency shares clinical features with autosomal dominant HIES because of signal transducer and activator of transcription 3 (STAT3) mutations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of T(H)17 cell dysfunction. The mechanisms underlying this phenotypic overlap are unclear. OBJECTIVE: We sought to elucidate common mechanisms operating in the different forms of HIES. METHODS: We analyzed the differentiation of CD4(+) T(H) cell subsets in control and DOCK8-deficient subjects. We also examined the role of DOCK8 in regulating STAT3 activation in T cells. T(H) cell differentiation was analyzed by ELISA, flow cytometry, and real-time PCR measurements of cytokines and T(H) cell transcription factors. The interaction of DOCK8 and STAT3 signaling pathways was examined by using flow cytometry, immunofluorescence, coimmunoprecipitation, and gene expression analysis. RESULTS: There was a profound block in the differentiation of DOCK8-deficient naive CD4(+) T cells into T(H)17 cells. A missense mutation that disrupts DOCK8 guanine nucleotide exchange factor (GEF) activity while sparing protein expression also impaired T(H)17 cell differentiation. DOCK8 constitutively associated with STAT3 independent of GEF activity, whereas it regulated STAT3 phosphorylation in a GEF activity-dependent manner. DOCK8 also promoted STAT3 translocation to the nucleus and induction of STAT3-dependent gene expression. CONCLUSION: DOCK8 interacts with STAT3 and regulates its activation and the outcome of STAT3-dependent T(H)17 differentiation. These findings might explain the phenotypic overlap between DOCK8 deficiency and autosomal dominant HIES. |Autoantibodies/immunology [MESH] |Cell Differentiation [MESH] |Child [MESH] |Child, Preschool [MESH] |Female [MESH] |Guanine Nucleotide Exchange Factors/*deficiency/genetics/*immunology/metabolism [MESH] |Humans [MESH] |Immunologic Deficiency Syndromes/genetics/*immunology/metabolism [MESH] |Infant [MESH] |Jurkat Cells [MESH] |Male [MESH] |Mutation [MESH] |Phosphorylation [MESH] |Protein Transport [MESH] |STAT3 Transcription Factor/*immunology/metabolism [MESH]Dedicator of cytokinesis 8 regulates signal transducer and activator o(epmc).pdf DeepDyve Pubget Overpricing