Dichotomous roles of co-stimulatory molecules in diabetes mellitus.

Dichotomous roles of co-stimulatory molecules in diabetes mellitus.
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DOI:
10.18632/oncotarget.23102
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发表时间:
2018-01-05
期刊:
影响因子:
--
通讯作者:
Duan L
Duan L
中科院分区:
其他
文献类型:
--
作者:
Zhong JX;Chen J;Rao X;Duan L

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许多研究已经确定了免疫功能障碍在糖尿病(包括1型和2型糖尿病)发展中的重要性,并且值得注意的是,T细胞活化在β细胞质量损失、脂肪炎症和胰岛素抵抗的发病机制中起关键作用。共刺激分子作为T细胞活化过程中的一个重要关卡,在糖尿病的发生发展中起着至关重要的作用。因此,阻断抗原提呈细胞与T细胞之间的共刺激二联体相互作用被认为是一种潜在的治疗策略。然而,研究也表明,某些共刺激分子的抑制或缺失并不一定能减少糖尿病的发生,甚至会加剧疾病的活动。在这里,在这种情况下,我们强调了共刺激分子相互作用在糖尿病发病机制中的二分作用。
Numerous studies have established the importance of immune dysfunction in the development of diabetes mellitus, including typ1 and typ2 diabetes, and it is worth noting that T cell activation acts a key role in the pathogenesis of loss of β cell mass, adipose inflammation and insulin resistance. Regarding as an important checkpoint in the process of T cell activation, co-stimulatory molecules interaction between antigen present cells and T cells have been identified the critical role in the development of diabetes mellitus. Thus, blockage of co-stimulatory dyads interaction between antigen present cells and T cells was supposed to a potential of therapeutic strategies. However, studies also showed that inhibition or deletion of some co-stimulatory molecules do not always reduce the development of diabetes, and even exacerbate the disease activity. Here, in this context, we highlight the dichotomous role of co-stimulatory molecules interaction in the pathogenesis of diabetes.
T细胞共刺激和共抑制的分子机制。
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