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10.1016/j.autrev.2014.01.050 http://scihub22266oqcxt.onion/10.1016/j.autrev.2014.01.050 C3995976!3995976!24424175     free     free     free       Autoimmun+Rev 2014 ; 13 (ä): 496-502 Nephropedia Template TP {{tp|p=24424175|t=2014. The IL-23/IL-17 Axis in Psoriatic Arthritis |pdf=|usr=}}{{24424175}} gab.com Text The IL-23/IL-17 Axis in Psoriatic Arthritis JO: Autoimmun Rev http://www.kidney.de/pget.php?&tw=1&pmid=24424175 #FOAvip Psoriatic arthritis (PsA) is an immune-mediated chronic inflammatory disease, affecting both the skin and joints. Disease progression is associated with aberrant cytokine expression, and TNF blockade is the most successful therapy to date. However, not all patients are responsive to anti-TNF treatment, highlighting the need to better understand the cellular and molecular mechanisms that govern the disease. PsA associations with single nucleotide polymorphisms in IL23R as well as TRAF3IP2 (Act1), a molecule downstream of the IL-17 receptor (IL-17R), have linked the IL-23/IL-17 axis to disease pathology. Although both cytokines are implicated in PsA, a full picture of their cellular targets and pathogenic mechanisms has not yet emerged. In this review, we focus on the IL-23/IL-17 axis-elicited responses mediated by osteoclasts, keratinocytes and neutrophils. Expanding our understanding of the cellular and molecular mechanisms that dictate pathogenicity in PsA will contribute to developing novel treatment strategies to combat disease. Twit Text FOAVip The IL-23/IL-17 Axis in Psoriatic Arthritis ????Autoimmun Rev http://www.kidney.de/pget.php?&tw=1&pmid=24424175 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24424175 #FOAvip English Wikipedia <ref>{{Cite pmid|24424175}}</ref> The IL-23/IL-17 Axis in Psoriatic Arthritis #MMPMID24424175 Suzuki E; Mellins ED; Gershwin ME; Nestle FO; Adamopoulos IE Autoimmun Rev 2014[Apr]; 13 (ä): 496-502 PMID24424175show ga Psoriatic arthritis (PsA) is an immune-mediated chronic inflammatory disease, affecting both the skin and joints. Disease progression is associated with aberrant cytokine expression, and TNF blockade is the most successful therapy to date. However, not all patients are responsive to anti-TNF treatment, highlighting the need to better understand the cellular and molecular mechanisms that govern the disease. PsA associations with single nucleotide polymorphisms in IL23R as well as TRAF3IP2 (Act1), a molecule downstream of the IL-17 receptor (IL-17R), have linked the IL-23/IL-17 axis to disease pathology. Although both cytokines are implicated in PsA, a full picture of their cellular targets and pathogenic mechanisms has not yet emerged. In this review, we focus on the IL-23/IL-17 axis-elicited responses mediated by osteoclasts, keratinocytes and neutrophils. Expanding our understanding of the cellular and molecular mechanisms that dictate pathogenicity in PsA will contribute to developing novel treatment strategies to combat disease. äThe IL-23/IL-17 Axis in Psoriatic Arthritis (epmc).pdf DeepDyve Pubget Overpricing