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10.3389/fimmu.2018.00200 http://scihub22266oqcxt.onion/10.3389/fimmu.2018.00200 C5834930!5834930!29535706     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       Front+Immunol 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=29535706|t=2018. IL-36? Is a Strong Inducer of IL-23 in Psoriatic Cells and Activates Angiogenesis |pdf=|usr=}}{{29535706}} gab.com Text IL-36 Is a Strong Inducer of IL-23 in Psoriatic Cells and Activates Angiogenesis JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29535706 #FOAvip The IL-1 family member cytokine IL-36? is recognised as key mediator in the immunopathology of psoriasis, hallmarks of which involve the activation of both resident and infiltrating inflammatory myeloid cells and aberrant angiogenesis. This research demonstrates a role for IL-36? in both myeloid activation and angiogenesis. We show that IL-36? induces the production of psoriasis-associated cytokines from macrophages (IL-23 and TNF?) and that this response is enhanced in macrophages from psoriasis patients. This effect is specific for IL-36? and could not be mimicked by other IL-1 family cytokines such as IL-1?. IL-36? was also demonstrated to induce endothelial tube formation and branching, in a VEGF-A-dependent manner. Furthermore, IL-36?-stimulated macrophages potently activated endothelial cells and led to increased adherence of monocytes, effects that were markedly more pronounced for psoriatic macrophages. Interestingly, regardless of stimulus, psoriasis monocytes showed increased adherence to both the stimulated and unstimulated endothelium when compared with monocytes from healthy individuals. Collectively, these findings show that IL-36? has the potential to enhance endothelium directed leucocyte infiltration into the skin and strengthen the IL-23/IL-17 pathway adding to the growing evidence of pathogenetic roles for IL-36? in psoriatic responses. Our findings also point to a cellular response, which could potentially explain cardiovascular comorbidities in psoriasis in the form of endothelial activation and increased monocyte adherence. Twit Text FOAVip IL-36 Is a Strong Inducer of IL-23 in Psoriatic Cells and Activates Angiogenesis ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=29535706 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29535706 #FOAvip English Wikipedia <ref>{{Cite pmid|29535706}}</ref> IL-36? Is a Strong Inducer of IL-23 in Psoriatic Cells and Activates Angiogenesis #MMPMID29535706 Bridgewood C; Fearnley GW; Berekmeri A; Laws P; Macleod T; Ponnambalam S; Stacey M; Graham A; Wittmann M Front Immunol 2018[]; 9 (ä): ä PMID29535706show ga The IL-1 family member cytokine IL-36? is recognised as key mediator in the immunopathology of psoriasis, hallmarks of which involve the activation of both resident and infiltrating inflammatory myeloid cells and aberrant angiogenesis. This research demonstrates a role for IL-36? in both myeloid activation and angiogenesis. We show that IL-36? induces the production of psoriasis-associated cytokines from macrophages (IL-23 and TNF?) and that this response is enhanced in macrophages from psoriasis patients. This effect is specific for IL-36? and could not be mimicked by other IL-1 family cytokines such as IL-1?. IL-36? was also demonstrated to induce endothelial tube formation and branching, in a VEGF-A-dependent manner. Furthermore, IL-36?-stimulated macrophages potently activated endothelial cells and led to increased adherence of monocytes, effects that were markedly more pronounced for psoriatic macrophages. Interestingly, regardless of stimulus, psoriasis monocytes showed increased adherence to both the stimulated and unstimulated endothelium when compared with monocytes from healthy individuals. Collectively, these findings show that IL-36? has the potential to enhance endothelium directed leucocyte infiltration into the skin and strengthen the IL-23/IL-17 pathway adding to the growing evidence of pathogenetic roles for IL-36? in psoriatic responses. Our findings also point to a cellular response, which could potentially explain cardiovascular comorbidities in psoriasis in the form of endothelial activation and increased monocyte adherence. äIL-36? Is a Strong Inducer of IL-23 in Psoriatic Cells and Activates A(epmc).pdf DeepDyve Pubget Overpricing