第三號誘餌受體在紅斑性狼瘡T細胞的活化及凋化所扮演之角色

Abstract

第三號誘餌受體 (DcR3) 是一個新定義的分子，屬於腫瘤壞死因子受體家族中的一員,它是FasL，LIGHT和TL1A的受體。然而對於可溶性DcR3的生物角色並不清楚，最近有一些文獻發現在紅斑性狼瘡 (SLE) 病人可以看到DcR3 mRNA的過度表現。在我們的研究中證明相較於正常人，在SLE病人的血清中的確有看到明顯增高的DcR3蛋白質，暗示著DcR3可能在SLE病人的生理及病理機轉扮演著某種角色。為了探討DcR3在SLE中可能影響的病理機轉，我們想要研究DcR3是否可能直接引起T細胞的活化，並且是否可能抑制活化T細胞所引起的細胞自發性死亡。在我們的結果證明可溶性DcR3與低濃度下的plate-bound anti-CD3抗體共同刺激下，可以增強人類T細胞的增殖，並且促進IL-2和IFN-

Decoy receptor 3 (DcR3), a newly member of tumor necrosis factor receptor (TNFR) superfamily, is a receptor for Fas ligand (FasL), LIGHT and TL1A. The biological role of soluble DcR3 is not clear, while DcR3 mRNA has been reported over-expressed in patients with systemic lupus erythematosus (SLE). Here we demonstrated marked elevated serum DcR3 in patients with SLE compared with normal health controls, suggested that DcR3 may play a role in SLE. In order to clarify the possible mechanisms in the pathogenesis of SLE by DcR3, we study whether DcR3 could directly induce T cell activation and whether it could promote survival of activated T cells via inhibiting the activation induced cell death (AICD). Our results demonstrated that soluble DcR3-Fc enhanced human T cell proliferation and increased production of IL-2 and IFN-