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• W2110252317 abstract "During the autoimmune response, when autoantigens are presented in addition to signals induced upon T-cell receptor engagement, T-cell activation requires the engagement of their costimulatory receptors by ligands on antigen-presenting cells (APCs) (1–3). The number of known costimulatory receptor/ligand pairs has grown significantly over the last decade (2,3), and it is now clear that costimulatory receptors can deliver signals either enhancing or inhibiting T-cell activation, thus determining the fate of the immune response (4). Classically, costimulatory molecule ligands were found on major histocompatibility complex (MHC) class II–expressing cells (so-called “professional APCs”), yet new data have demonstrated parenchymal expression of costimulatory ligands (e.g., in pancreatic islets) (5), thus providing a second level of immune response regulation in situ (6).Many players appear to have a role in the interaction between the immune system and β-cells: the classical costimulatory molecule B7.1 (or CD80), a receptor expressed by APCs and parenchymal cells that engages the T-cell ligand CD28 and thus activates the immune system (9); programmed death receptor-1 (PD-1), an inhibitory receptor induced on activated T-, B-, and myeloid cells; and finally, the ligand for PD-1 (PD-L1 or B7-H1), which is constitutively expressed in parenchymal organs (10–12). Triggering negative signals through the interaction of PD-1 and PD-L1 could inhibit T-cell activation as well as the migration of T-cells into peripheral tissues (10–13). In NOD mice, islet PD-L1 expression has been shown to protect …" @default.
• W2110252317 created "2016-06-24" @default.
• W2110252317 creator A5028314110 @default.
• W2110252317 date "2010-08-01" @default.
• W2110252317 modified "2023-09-23" @default.
• W2110252317 title "β-Cells Step Up in Controlling the Autoimmune Response" @default.
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• W2110252317 doi "https://doi.org/10.2337/db10-0662" @default.
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