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RISS 인기검색어
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- 저자 : ( Siba P. Raychaudhuri ) (검색결과 2 건)
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Is It Possible to Discontinue Tumor Necrosis Factor Antagonists after Psoriasis Remission?
( Byungsoo Kim ),( Emanual Maverakis ),( Siba P. Raychaudhuri ) 대한피부과학회 2019 Annals of Dermatology Vol.31 No.5
Tumor necrosis factor (TNF) antagonists are highly effective treatments for psoriasis. These agents provide the opportunity to improve disease activity and achieve clinical remission. Despite its efficacy, long-term use of biologics is associated with high financial costs and possibly life-threatening adverse events. Recently, there has been an increasing interest in discontinuing TNF antagonists in patients with psoriasis who have achieved a positive clinical response. However, there is a paucity of data and clinical guidelines concerning the cessation TNF antagonists in psoriasis treatment. Several factors, including cost, subsequent treatment efficacy, relative risks, and tolerability, should be considered before the decision is made to discontinue TNF antagonists. Well-designed clinical trials are necessary to identify factors that may trigger disease exacerbation after medication discontinuation in order to recognize the potential disadvantages of discontinuing treatment in patients who are previously successfully managed on TNF antagonists. (Ann Dermatol 31(5) 495∼501, 2019)
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( Byungsoo Kim ),( Soumajyoti Sarkar ),( Christine Abria ),( Smriti K. Raychaudhuri ),( Siba P. Raychaudhuri ) 대한피부과학회 2019 대한피부과학회 학술발표대회집 Vol.71 No.2
Background: IL-17A, IL-22 and TNF- α play leading roles in Psoriatic arthritis (PsA) but their regulatory role on JAK-STAT signaling for pannus formation remains unknown. Objectives: To address whether the key regulatory cytokines of PsA induce phosphorylation of STAT3 and can JAK-STAT inhibitor antagonize effects on pannus formation induced by TNF- α, IL-17 and IL-22. Methods: We tested the effect of tofacitinib on the IL-6, IL-8 and MMP-3 production in FLS. FLS were cultured with TNF-α, IL-17A or IL-22 and ELISAs were performed for IL-6, IL-8 and MMP-3. MTT assay was done for proliferation and immunoblot studies of FLS lysates were done for STAT3. Results: IL-17, IL-22, TNF-α induced phosphorylation of STAT3. PsA FLS pre-treated with tofacitinib showed decreased levels of phospho-STAT3 compared to the FLS cells without tofacitinib. IL-17, TNF-α and IL-22 induced significant proliferation of PsA and RA FLS. PsA and RA FLS stimulated with IL-17A, IL-22 or TNF-α produced significantly more IL-6 IL-8 and MMP-3 compared to media and that could be reduced when these FLS were pre-treated with tofacitinib. Conclusion: FLS proliferation, IL-6, IL-8 and MMP-3 production by FLS are the two critical events of pannus formation induced by IL-17A, TNF-α and IL-22 and is regulated by the JAK-STAT kinase system. These data support a role for JAK-STAT signaling pathways in PsA and provides mechanisms of actions of tofacitinib for its efficacy.
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