CAJ | 학술논문

寻常性银屑病是一种多基因遗传性疾病,近年来,深入的遗传学分析及免疫学分析表明,调节白介素23/Th17、Th1-Th2-Th17及核因子-κB途径是导致银屑病的危险因素.在皮损处,这些炎症通路中各种细胞因子(如白介素17和22)的分泌增多.在不加干预的情况下,银屑病中一系列有活性的炎症性细胞因子可能触发炎症反应和细胞增生的恶性循环,最终导致皮损形成.深入了解这些途径可从遗传学和免疫学的层面为治疗疾病奠定基础.
심상성은설병시일충다기인유전성질병,근년래,심입적유전학분석급면역학분석표명,조절백개소23/Th17、Th1-Th2-Th17급핵인자-κB도경시도치은설병적위험인소.재피손처,저사염증통로중각충세포인자(여백개소17화22)적분비증다.재불가간예적정황하,은설병중일계렬유활성적염증성세포인자가능촉발염증반응화세포증생적악성순배,최종도치피손형성.심입료해저사도경가종유전학화면역학적층면위치료질병전정기출.
Psoriasis vulgaris is a multifactorial genetic disease.Recent advances in genetic and immunological studies have revealed that the changes in interleukin (IL)-23/T helper type 17 (Th17) cells,Th1-Th2-Th17 and nuclear factor-κB pathways are risk factors for psoriasis.The secretion of various cytokines (such as IL-17 and IL-22) involved in these pathways is increased in psoriatic lesions.Unrestrained,the activated inflammatory cytokines network in psoriasis may trigger a vicious cycle of inflammation and cellular proliferation that ultimately results in lesion formation.Deeply understanding these pathways may pave the path to tailor treatment on the basis of an individual's genetic and immunologic profile.