国际生物制品学杂志
國際生物製品學雜誌
국제생물제품학잡지
INTERNATIONAL JOURNAL OF BIOLOGICALS
2010年
1期
38-43,46
,共7页
肿瘤坏死因子α%关节炎,类风湿%抗TNFα药物
腫瘤壞死因子α%關節炎,類風濕%抗TNFα藥物
종류배사인자α%관절염,류풍습%항TNFα약물
Tumor necrosis factor-alpha%Arthritis%rheumatoid%Anti-TNFα agents
肿瘤坏死因子α(tumor necrosis factor alpha,TNFα)是一种具有多效生物活性的细胞因子,能够引起细胞凋亡、细胞增殖、分化、促炎症反应和免疫调节等作用.TNFα在类风湿关节炎(rheumatoid arthritis,RA)的致病机制中起关键作用.TNFα与TNF受体结合,能够引起细胞内的信号传导,通过复杂的级联反应和信号网络,激活转录因子核因子-κβ(nuclear factor-kappa B,NF-κβ)和活化蛋白-1(acti-vator protein-1,AP-1),调控目的基因的表达,造成炎症反应和骨关节损伤.而以TNFα为靶位的药物已经被开发并应用于RA的临床治疗,通过阻断TNFα引起的信号传导来降低炎症反应被证明是安全有效的.此文就TNFα在RA病理机制中的作用及抗TNFα药物的进展作一综述.
腫瘤壞死因子α(tumor necrosis factor alpha,TNFα)是一種具有多效生物活性的細胞因子,能夠引起細胞凋亡、細胞增殖、分化、促炎癥反應和免疫調節等作用.TNFα在類風濕關節炎(rheumatoid arthritis,RA)的緻病機製中起關鍵作用.TNFα與TNF受體結閤,能夠引起細胞內的信號傳導,通過複雜的級聯反應和信號網絡,激活轉錄因子覈因子-κβ(nuclear factor-kappa B,NF-κβ)和活化蛋白-1(acti-vator protein-1,AP-1),調控目的基因的錶達,造成炎癥反應和骨關節損傷.而以TNFα為靶位的藥物已經被開髮併應用于RA的臨床治療,通過阻斷TNFα引起的信號傳導來降低炎癥反應被證明是安全有效的.此文就TNFα在RA病理機製中的作用及抗TNFα藥物的進展作一綜述.
종류배사인자α(tumor necrosis factor alpha,TNFα)시일충구유다효생물활성적세포인자,능구인기세포조망、세포증식、분화、촉염증반응화면역조절등작용.TNFα재류풍습관절염(rheumatoid arthritis,RA)적치병궤제중기관건작용.TNFα여TNF수체결합,능구인기세포내적신호전도,통과복잡적급련반응화신호망락,격활전록인자핵인자-κβ(nuclear factor-kappa B,NF-κβ)화활화단백-1(acti-vator protein-1,AP-1),조공목적기인적표체,조성염증반응화골관절손상.이이TNFα위파위적약물이경피개발병응용우RA적림상치료,통과조단TNFα인기적신호전도래강저염증반응피증명시안전유효적.차문취TNFα재RA병리궤제중적작용급항TNFα약물적진전작일종술.
Tumor necrosis factor alpha (TNFα) is a pleiotropic cytokine that mediates diverse biological effects, including apoptosis, cell proliferation, differentiation, proinflammatory reaction and immunoregulation.TNFα is known to play a critical role in the pathogenic mechanism of rheumatoid arthritis (RA).Binding of TNFα to TNF receptor (TNFR) results in transduction of cellular signal.Through complex signaling cascades and networks, transcription factors NF-κβ and AP-1 are activated to regulate target gene expression,resulting in joint inflammation and damage.Drugs targeting TNFα have been developed to reduce the injurious effects of proinflammatory cytokine and have proved to be safe and effective in the treatment of patients with RA.This article reviews the role of TNFα in pathogenic mechanism of RA and recent progress of antiTNFα agents.