美國國立衛(wèi)生研究所下屬國立關(guān)節(jié)炎和肌肉骨骼、皮膚疾病研究中心（NIAMS）一項研究，發(fā)現(xiàn)了自體免疫病的一種有前途的治療靶位——細胞的表面受體DR3。研究結(jié)果發(fā)表在《免疫》（ Immunity ）上。
研究者們以小鼠為動物模型進行試驗，研究表明阻斷這一受體可以延緩或是停止自體免疫疾病炎癥對機體的損傷，更是可以使機體免受其他嚴(yán)重傳染病的感染，先階段的治療往往無法避免其他傳染病的感染。
DR3是細胞表面的一種蛋白，是腫瘤壞死因子（TNF）受體成員中的一種，它可與TNF相關(guān)的分子結(jié)合，TNF是一種細胞信號蛋白，TNF可促進炎癥反應(yīng)?，F(xiàn)在很多治療炎癥疾病（如類風(fēng)濕性關(guān)節(jié)炎、牛皮癬）的方法都是阻斷TNF，以達到阻斷炎癥的目的。但是，抗TNF的治療方法并不是對所有的自體免疫疾病都有效，因此研究人員轉(zhuǎn)向研究DR3，DR3與TNFR1（1型腫瘤壞死因子受體）有密切的關(guān)系，TNFR1是腫瘤壞死因子的主要受體。（生物谷Bioon.com）
生物谷推薦原始出處：
Immunity ，doi：10.1016/j.immuni.2008.04.021，F(xiàn)ran?oise Meylan，Richard M. Siegel
Françoise Meylan,1 Todd S. Davidson,2 Erin Kahle,1 Michelle Kinder,1 Krishika Acharya,1 Dragana Jankovic,3 Virgilio Bundoc,4 Marcus Hodges,4 Ethan M. Shevach,2 Andrea Keane-Myers,4 Eddie C.Y. Wang,5 and Richard M. Siegel1,
ImmunoregulationUnit, Autoimmunity Branch, National Institute of Arthritis andMusculoskeletal and Skin Diseases, National Institutes of Health,Bethesda, MD 20892
2 CellularImmunology Section, Laboratory of Immunology, National Institute ofAllergy and Infectious Diseases, National Institutes of Health,Bethesda, MD 20892
3 ImmunobiologySection, Laboratory of Parasitic Diseases, National Institute ofAllergy and Infectious Diseases, National Institutes of Health,Bethesda, MD 20892
4 AllergicInflammation Section, Laboratory of Allergic Diseases, NationalInstitute of Allergy and Infectious Diseases, National Institutes ofHealth, Bethesda, MD 20892
5 School of Medicine, Cardiff University, Cardiff CF14 4XN, Wales, UK
Summary
DR3 (TRAMP, LARD, WSL-1,TNFRSF25) is a death-domain-containing tumor necrosis factor(TNF)-family receptor primarily expressed on T cells. TL1A, theTNF-family ligand for DR3, can costimulate T cells, but thephysiological function of TL1A-DR3 interactions in immune responses isnot known. Using DR3-deficient mice, we identified DR3 as the receptorresponsible for TL1A-induced T cell costimulation and dendritic cells asthe likely source for TL1A during T cell activation. Despite its rolein costimulation, DR3 was not required for in vivo T cell priming, forpolarization into T helper 1 (Th1), Th2, or Th17 effector cell subtypes,or for effective control of infection with Toxoplasma gondii.Instead, DR3 expression was required on T cells for immunopathology,local T cell accumulation, and cytokine production in ExperimentalAutoimmune Encephalomyelitis (EAE) and allergic lung inflammation,disease models that depend on distinct effector T cell subsets. DR3could be an attractive therapeutic target for T cell-mediated autoimmuneand allergic diseases.
