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10.1186/ar4499 http://scihub22266oqcxt.onion/10.1186/ar4499 C4060204!4060204 !24598455     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24598455 &cmd=llinks): Failed to open stream: HTTP request failed! 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T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus? |pdf=|usr=}}{{24598455 }} gab.com Text T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus JO: Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=24598455 #FOAvip INTRODUCTION: A hallmark of systemic autoimmune diseases like systemic lupus erythematosus (SLE) is the increased expression of interferon (IFN) type I inducible genes, so-called IFN type I signature. Recently, T-helper 17 subset (Th17 cells), which produces IL-17A, IL-17F, IL-21, and IL-22, has been implicated in SLE. As CCR6 enriches for Th17 cells, we used this approach to investigate whether CCR6? memory T-helper cells producing IL-17A, IL-17F, IL-21, and/or IL-22 are increased in SLE patients and whether this increase is related to the presence of IFN type I signature. METHODS: In total, 25 SLE patients and 15 healthy controls (HCs) were included. SLE patients were divided into IFN type I signature-positive (IFN?) (n?=?16) and negative (IFN?) (n?=?9) patients, as assessed by mRNA expression of IFN-inducible genes (IFIGs) in monocytes. Expression of IL-17A, IL-17F, IL-21, and IL-22 by CD4?CD45RO?CCR6? T cells (CCR6? cells) was measured with flow cytometry and compared between IFN?, IFN? patients and HCs. RESULTS: Increased percentages of IL-17A and IL-17A/IL-17F double-producing CCR6? cells were observed in IFN? patients compared with IFN? patients and HCs. IL-17A and IL-17F expression within CCR6? cells correlated significantly with IFIG expression. In addition, we found significant correlation between B-cell activating factor of the tumor necrosis family (BAFF)-a factor strongly correlating with IFN type I?-?and IL-21 producing CCR6? cells. CONCLUSIONS: We show for the first time higher percentages of IL-17A and IL-17A/IL-17F double-producing CCR6? memory T-helper cells in IFN? SLE patients, supporting the hypothesis that IFN type I co-acts with Th17 cytokines in SLE pathogenesis. Twit Text FOAVip T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus ????Arthritis Res Ther http://www.kidney.de/pget.php?&tw=1&pmid=24598455 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24598455 #FOAvip English Wikipedia <ref>{{Cite pmid|24598455 }}</ref> T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus? #MMPMID24598455 Brkic Z ; Corneth OB ; van Helden-Meeuwsen CG ; Dolhain RJ ; Maria NI ; Paulissen SM ; Davelaar N ; van Hamburg JP ; van Daele PL ; Dalm VA ; van Hagen PM ; Hazes JM ; Versnel MA ; Lubberts E Arthritis Res Ther 2014[Mar]; 16 (2 ): R62 PMID24598455 show ga INTRODUCTION: A hallmark of systemic autoimmune diseases like systemic lupus erythematosus (SLE) is the increased expression of interferon (IFN) type I inducible genes, so-called IFN type I signature. Recently, T-helper 17 subset (Th17 cells), which produces IL-17A, IL-17F, IL-21, and IL-22, has been implicated in SLE. As CCR6 enriches for Th17 cells, we used this approach to investigate whether CCR6? memory T-helper cells producing IL-17A, IL-17F, IL-21, and/or IL-22 are increased in SLE patients and whether this increase is related to the presence of IFN type I signature. METHODS: In total, 25 SLE patients and 15 healthy controls (HCs) were included. SLE patients were divided into IFN type I signature-positive (IFN?) (n?=?16) and negative (IFN?) (n?=?9) patients, as assessed by mRNA expression of IFN-inducible genes (IFIGs) in monocytes. Expression of IL-17A, IL-17F, IL-21, and IL-22 by CD4?CD45RO?CCR6? T cells (CCR6? cells) was measured with flow cytometry and compared between IFN?, IFN? patients and HCs. RESULTS: Increased percentages of IL-17A and IL-17A/IL-17F double-producing CCR6? cells were observed in IFN? patients compared with IFN? patients and HCs. IL-17A and IL-17F expression within CCR6? cells correlated significantly with IFIG expression. In addition, we found significant correlation between B-cell activating factor of the tumor necrosis family (BAFF)-a factor strongly correlating with IFN type I?-?and IL-21 producing CCR6? cells. CONCLUSIONS: We show for the first time higher percentages of IL-17A and IL-17A/IL-17F double-producing CCR6? memory T-helper cells in IFN? SLE patients, supporting the hypothesis that IFN type I co-acts with Th17 cytokines in SLE pathogenesis. |Adult [MESH] |Cytokines/*immunology [MESH] |Female [MESH] |Flow Cytometry [MESH] |Humans [MESH] |Interferon Type I/*immunology [MESH] |Lupus Erythematosus, Systemic/*immunology [MESH] |Male [MESH] |Real-Time Polymerase Chain Reaction [MESH]T-helper 17 cell cytokines and interferon type I: partners in crime in(epmc).pdf DeepDyve Pubget Overpricing