Kaminitz Ayelet, Stein Jerry, Yaniv Isaac, Askenasy Nadir
Frankel Laboratory, Center for Stem Cell Research, Schneider Children's Medical Center of Israel, Petach Tikva, Israel.
Immunol Cell Biol. 2007 Nov-Dec;85(8):582-9. doi: 10.1038/sj.icb.7100093. Epub 2007 Jul 17.
Autoimmune insulitis, the cause of type 1 diabetes, evolves through several discrete stages that culminate in beta-cell death. In the first stage, antigenic epitopes of B-cell-specific peptides are processed by antigen presenting cells in local lymph nodes, and auto-reactive lymphocyte clones are propagated. Subsequently, cell-mediated and direct cytokine-mediated reactions are generated against the beta-cells, and the beta-cells are sensitized to apoptosis. Ironically, the beta-cells themselves contribute some of the cytokines and chemokines that provoke the immune reaction within the islets. Once this vicious cycle of autoimmunity is fully developed, the fate of the beta-cells in the islets is sealed, and clinical diabetes inevitably ensues. Differences in various aspects of these concurrent events appear to underlie the significant discrepancies in experimental data observed in experimental models that simulate autoimmune insulitis.
自身免疫性胰岛炎是1型糖尿病的病因，它通过几个离散阶段发展，最终导致β细胞死亡。在第一阶段，B细胞特异性肽的抗原表位由局部淋巴结中的抗原呈递细胞处理，自身反应性淋巴细胞克隆得以增殖。随后，针对β细胞产生细胞介导和直接细胞因子介导的反应，β细胞对凋亡敏感。具有讽刺意味的是，β细胞自身会产生一些引发胰岛内免疫反应的细胞因子和趋化因子。一旦这种自身免疫的恶性循环完全形成，胰岛中β细胞的命运就已注定，临床糖尿病不可避免地随之而来。这些并发事件在各个方面的差异似乎是模拟自身免疫性胰岛炎的实验模型中观察到的实验数据存在显著差异的原因。
