The Mina & Everard Goodman Faculty of Life Sciences, The Safdiè AIDS and Immunology Research Center, C.A.I.R. Institute, Ramat Gan, Israel.
Interdisciplinary Department, Bar-Ilan University, Ramat Gan, Israel.
Front Immunol. 2019 May 29;10:979. doi: 10.3389/fimmu.2019.00979. eCollection 2019.
The study shows that treatment of NOD mice with either of two tellurium-based small molecules, AS101 [ammonium trichloro(dioxoethylene-o,o')tellurate] or SAS [octa-O-bis-(R,R)-tartarate ditellurane] could preserve β cells function and mass. These beneficial effects were reflected in decreased incidence of diabetes, improved glucose clearance, preservation of body weight, and increased survival. The normal glucose levels were associated with increased insulin levels, preservation of β cell mass and increased islet size. Importantly, this protective activity could be demonstrated when the compounds were administered either at the early pre-diabetic phase with no or initial insulitis, at the pre-diabetic stage with advanced insulitis, or even at the advanced, overtly diabetic stage. We further demonstrate that both tellurium compounds prevent migration of autoimmune lymphocytes to the pancreas, via inhibition of the α4β7 integrin activity. Indeed, the decreased migration resulted in diminished pancreatic islets damage both with respect to their size, β cell function, and caspase-3 activity, the hallmark of apoptosis. Most importantly, AS101 and SAS significantly elevated the number of T regulatory cells in the pancreas, thus potentially controlling the autoimmune process. We show that the compounds inhibit pancreatic caspase-1 activity followed by decreased levels of the inflammatory cytokines IL-1β and IL-17 in the pancreas. These properties enable the compounds to increase the proportion of Tregs in the pancreatic lymph nodes. AS101 and SAS have been previously shown to regulate specific integrins through a unique redox mechanism. Our current results suggest that amelioration of disease in NOD mice by this unique mechanism is due to decreased infiltration of pancreatic islets combined with increased immune regulation, leading to decreased inflammation within the islets. As these tellurium compounds show remarkable lack of toxicity in clinical trials (AS101) and pre-clinical studies (SAS), they may be suitable for the treatment of type-1 diabetes.
研究表明,用两种基于碲的小分子化合物中的任何一种治疗 NOD 小鼠,AS101[三氯(二氧代乙烯-O,O')碲酸铵]或 SAS[八-O-双(R,R)-酒石酸二碲烷],都可以维持β细胞的功能和质量。这些有益的效果反映在糖尿病发病率降低、葡萄糖清除率提高、体重保持和存活率增加上。正常的血糖水平与胰岛素水平升高、β细胞质量增加和胰岛增大有关。重要的是,当化合物在没有或最初的胰岛炎的早期糖尿病前期阶段、在有晚期胰岛炎的糖尿病前期阶段,甚至在晚期、明显的糖尿病阶段给药时,都可以观察到这种保护活性。我们进一步证明,这两种碲化合物通过抑制α4β7 整合素活性,防止自身免疫性淋巴细胞向胰腺迁移。事实上,迁移减少导致胰腺胰岛的损伤减少,无论是在其大小、β细胞功能还是半胱天冬酶-3 活性方面,这些都是细胞凋亡的标志。最重要的是,AS101 和 SAS 显著增加了胰腺中的 T 调节细胞数量,从而潜在地控制了自身免疫过程。我们发现,这些化合物抑制胰腺半胱天冬酶-1 的活性,随后降低了胰腺中炎症细胞因子 IL-1β 和 IL-17 的水平。这些特性使化合物能够增加胰腺淋巴结中 Tregs 的比例。AS101 和 SAS 之前被证明通过独特的氧化还原机制调节特定的整合素。我们目前的结果表明,这种独特机制改善 NOD 小鼠的疾病是由于胰腺胰岛浸润减少和免疫调节增加导致胰岛内炎症减少所致。由于这些碲化合物在临床试验(AS101)和临床前研究(SAS)中表现出显著的无毒副作用,它们可能适合治疗 1 型糖尿病。