select ad.sno,ad.journal,ad.title,ad.author_names,ad.abstract,ad.abstractlink,j.j_name,vi.* from articles_data ad left join journals j on j.journal=ad.journal left join vol_issues vi on vi.issue_id_en=ad.issue_id where ad.sno_en='48063' and ad.lang_id='8' and j.lang_id='8' and vi.lang_id='8' The Role of T-Cell Costimulatory Pathways in Regulation of A | 48063
क्लिनिकल और सेलुलर इम्यूनोलॉजी जर्नल

क्लिनिकल और सेलुलर इम्यूनोलॉजी जर्नल
खुला एक्सेस

आईएसएसएन: 2155-9899

अमूर्त

The Role of T-Cell Costimulatory Pathways in Regulation of Autoimmune Diabetes

I-Fang Lee, Dawei Ou, Daniel L. Metzger and Garth L. Warnock

Many factors contribute to the pathogenesis of autoimmune diabetes. Targets for treating this debilitating disease will become more apparent by understanding the nature of immune activation. This review examines the possibility of targeting costimulation and discusses the molecules found on the T cell and the antigen-presenting cell (APC) that participate in T-cell activation. The B7-1/B7-2:CD28/cytotoxic T lymphocyte antigen-4 (CTLA-4) pathway has been shown to be crucial in regulating T-cell activation and tolerance. Novel members of the B7-CD28 superfamily have recently been discovered, and they appear to be particularly important for regulating the responses of previously activated T cells. Superimposition of inhibitory signals, such as those delivered by CTLA-4 and the programmed death (PD)-1-PD-1 ligand (PD-L1) pathway, leads to a complex network of positive and negative costimulatory signals, the integration of which modulates immune responses. Furthermore, expression of the B7 homolog B7-H4 on cells in peripheral tissues indicates new mechanisms for regulating T-cell responses. This review focuses on our current understanding of the members of the B7:CD28 superfamily and discusses their therapeutic potential in autoimmune diabetes.

अस्वीकरण: इस सार का अनुवाद कृत्रिम बुद्धिमत्ता उपकरणों का उपयोग करके किया गया था और अभी तक इसकी समीक्षा या सत्यापन नहीं किया गया है।
Top