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10.1002/art.40014 http://scihub22266oqcxt.onion/10.1002/art.40014 C5526072!5526072!27992687     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27992687&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 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       Arthritis+Rheumatol 2017 ; 69 (4): 808-13 Nephropedia Template TP {{tp|p=27992687|t=2017. CD4+ T cells from SLE patients respond poorly to exogenous IL-2 |pdf=|usr=}}{{27992687}} gab.com Text CD4+ T cells from SLE patients respond poorly to exogenous IL-2 JO: Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=27992687 #FOAvip Objective: Imbalanced cytokine production by T cells characterizes both patients with SLE and lupus-prone mice and contributes to immune dysregulation. In this study, we further characterize in detail the production of IL-2, IFN?, IL-4 and IL-17A by CD4+ subsets in healthy subjects and SLE patients and the signaling response of CD4+ T cells in response to exogenous IL-2. Methods: Cytokine production by CD4+ T cell differentiated subsets was assessed by intracellular staining following stimulation with phorbol myristate acetate and ionomycin and by ELISA after anti-CD3/anti-CD28 stimulation. IL-2 signaling pathway was examined by assessing Jak3 and STAT5 phosphorylation. Cell proliferation in response to IL-2 was examined by CFSE dilution. Results: Production of IL-2 was defective primarily among naïve CD4+ T cell, whereas the production of IFN?, IL-4 and IL-17A was not significantly different among SLE patients and healthy subjects. Jak3 and STAT5 phosphorylation and proliferation of SLE CD4+ T cells in response to exogenous IL-2 were impaired compared to that of healthy subjects. Conclusion: These data suggest that altered IL-2 production, as well as impaired IL-2-mediated signaling and proliferative responses characterize SLE CD4+ T cells. Our data suggest caution in designing IL-2 treatment trials for patients with SLE. Approaches to restore CD4+ T cell sensitivity to IL-2 should be considered along the way. Twit Text FOAVip CD4+ T cells from SLE patients respond poorly to exogenous IL-2 ????Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=27992687 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27992687 #FOAvip English Wikipedia <ref>{{Cite pmid|27992687}}</ref> CD4+ T cells from SLE patients respond poorly to exogenous IL-2 #MMPMID27992687 Comte D; Karampetsou MP; Kis-Toth K; Yoshida N; Bradley SJ; Kyttaris VC; Tsokos GC Arthritis Rheumatol 2017[Apr]; 69 (4): 808-13 PMID27992687show ga Objective: Imbalanced cytokine production by T cells characterizes both patients with SLE and lupus-prone mice and contributes to immune dysregulation. In this study, we further characterize in detail the production of IL-2, IFN?, IL-4 and IL-17A by CD4+ subsets in healthy subjects and SLE patients and the signaling response of CD4+ T cells in response to exogenous IL-2. Methods: Cytokine production by CD4+ T cell differentiated subsets was assessed by intracellular staining following stimulation with phorbol myristate acetate and ionomycin and by ELISA after anti-CD3/anti-CD28 stimulation. IL-2 signaling pathway was examined by assessing Jak3 and STAT5 phosphorylation. Cell proliferation in response to IL-2 was examined by CFSE dilution. Results: Production of IL-2 was defective primarily among naïve CD4+ T cell, whereas the production of IFN?, IL-4 and IL-17A was not significantly different among SLE patients and healthy subjects. Jak3 and STAT5 phosphorylation and proliferation of SLE CD4+ T cells in response to exogenous IL-2 were impaired compared to that of healthy subjects. Conclusion: These data suggest that altered IL-2 production, as well as impaired IL-2-mediated signaling and proliferative responses characterize SLE CD4+ T cells. Our data suggest caution in designing IL-2 treatment trials for patients with SLE. Approaches to restore CD4+ T cell sensitivity to IL-2 should be considered along the way. äCD4+ T cells from SLE patients respond poorly to exogenous IL-2 (epmc).pdf DeepDyve Pubget Overpricing