安徽医药
安徽醫藥
안휘의약
ANHUI MEDICAL AND PHARMACEUTICAL JOURNAL
2015年
6期
1021-1024
,共4页
TLR2%TLR4%类风湿关节炎
TLR2%TLR4%類風濕關節炎
TLR2%TLR4%류풍습관절염
Toll like receptor 2%Toll like receptor 4%rheumatoid arthritis
Toll样受体（TLRs）是天然免疫系统中特异性的Ⅰ型跨膜受体及病原模式识别受体，在急性炎症反应、细胞信号转导和细胞凋亡中起重要作用。TLRs通过选择性的识别病原体中病原相关分子模式的保守结构及某些内源性配体，触发髓样细胞分化因子88（MyD88）依赖性和非依赖性途径，导致基因编码的的促炎性细胞因子和趋化因子的激活，从而诱发局部的炎症，并通过上调抗原递呈细胞表面的共刺激分子，诱导T、B淋巴细胞分化，激动后继的适应性免疫应答。类风湿关节炎（RA ）主要表现为滑膜组织炎性增生和炎症细胞浸润最终导致组织破坏和功能障碍。与T细胞过度活化以及B细胞的过度刺激致大量自身抗体产生有关。研究发现，细胞表面的TLRs，尤其是TLR2和TLR4，在类风湿关节炎疾病的发生发展中起重要作用。该文就TLR2、TLR4在RA发病中的作用作一综述，旨在为后期药物干预提供一定的理论依据。
Toll樣受體（TLRs）是天然免疫繫統中特異性的Ⅰ型跨膜受體及病原模式識彆受體，在急性炎癥反應、細胞信號轉導和細胞凋亡中起重要作用。TLRs通過選擇性的識彆病原體中病原相關分子模式的保守結構及某些內源性配體，觸髮髓樣細胞分化因子88（MyD88）依賴性和非依賴性途徑，導緻基因編碼的的促炎性細胞因子和趨化因子的激活，從而誘髮跼部的炎癥，併通過上調抗原遞呈細胞錶麵的共刺激分子，誘導T、B淋巴細胞分化，激動後繼的適應性免疫應答。類風濕關節炎（RA ）主要錶現為滑膜組織炎性增生和炎癥細胞浸潤最終導緻組織破壞和功能障礙。與T細胞過度活化以及B細胞的過度刺激緻大量自身抗體產生有關。研究髮現，細胞錶麵的TLRs，尤其是TLR2和TLR4，在類風濕關節炎疾病的髮生髮展中起重要作用。該文就TLR2、TLR4在RA髮病中的作用作一綜述，旨在為後期藥物榦預提供一定的理論依據。
Toll양수체（TLRs）시천연면역계통중특이성적Ⅰ형과막수체급병원모식식별수체，재급성염증반응、세포신호전도화세포조망중기중요작용。TLRs통과선택성적식별병원체중병원상관분자모식적보수결구급모사내원성배체，촉발수양세포분화인자88（MyD88）의뢰성화비의뢰성도경，도치기인편마적적촉염성세포인자화추화인자적격활，종이유발국부적염증，병통과상조항원체정세포표면적공자격분자，유도T、B림파세포분화，격동후계적괄응성면역응답。류풍습관절염（RA ）주요표현위활막조직염성증생화염증세포침윤최종도치조직파배화공능장애。여T세포과도활화이급B세포적과도자격치대량자신항체산생유관。연구발현，세포표면적TLRs，우기시TLR2화TLR4，재류풍습관절염질병적발생발전중기중요작용。해문취TLR2、TLR4재RA발병중적작용작일종술，지재위후기약물간예제공일정적이론의거。
Toll like receptors(TLRs)are pattern recognition receptors belonging to innate immunity and the typeⅠtransmenbrane glyco-protein receptor family that play an essential role in inflammation,cells signal transduction and apoptosis.Besides these exogenous pathogen-associated molecular patterns,TLRs can also bind with these endogenous ligands.By combine with their ligands,extracelluar signals enter into cell and activate the trigger the Myeloid differentiation factor 88 (MyD88 )in dependent or independent pathway, cause the activation of inflammatory cytokines and chemokines,lead to the host’s inflammatory response.Besides,the signals can also upregulate the costimulatory molecules on the surfaces of antigen-presenting cells,induce the differentiation of T or B lymphocytes,ex-cite the following adaptive immune response.Rheumatoid arthritis (RA)is a chronic autoimmune disease,characterized by cytokines-mediated inflammation of the synovial lining of joints and destruction of cartilage and bone.It was related with the T cell hyperactivity and B cell overstimulation leading to overproduction of autoantibodies.Study found that TLRs,especially the TLR2 and TLR4,play a critical action in RA.In this review,to provide a theoretical basis for further drug intervention study we summarized the TLR2/4and their function in RA.
