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通过使用TCR转基因小鼠剖析CD4 + T细胞在自身免疫性糖尿病中的作用。

Dissecting the role of CD4+ T cells in autoimmune diabetes through the use of TCR transgenic mice.

作者信息

Suri A, Katz J D

机构信息

Department of Pathology, Center for Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

出版信息

Immunol Rev. 1999 Jun;169:55-65. doi: 10.1111/j.1600-065x.1999.tb01306.x.

Abstract

Insulin-dependent diabetes mellitus (IDDM) is an immunological disorder wherein autoimmune-mediated destruction of islet cells in the pancreas results in persistent hyperglycemia. The non-obese diabetic mouse model of IDDM has revealed the importance of multiple factors that impact upon the disease process; however, understanding of primary immune mechanisms leading to IDDM remains elusive. The emergence of transgenic mouse models for IDDM has made important contributions towards clarifying many of these factors, including the cell types, the various effector molecules and the genetic elements involved in the pathogenesis of IDDM. In this review, we will focus on the primary mechanism and mediators of islet beta-cell death, the impact of T-helper lymphocytes on disease progression and the potential role of major histocompatibility complex class II molecules in conferring susceptibility to IDDM.

摘要

胰岛素依赖型糖尿病(IDDM)是一种免疫紊乱疾病,其中胰腺中胰岛细胞的自身免疫介导性破坏会导致持续性高血糖。IDDM的非肥胖糖尿病小鼠模型揭示了多种影响疾病进程的因素的重要性;然而,对导致IDDM的主要免疫机制的理解仍然难以捉摸。IDDM转基因小鼠模型的出现为阐明许多这些因素做出了重要贡献,包括细胞类型、各种效应分子以及参与IDDM发病机制的遗传元件。在本综述中,我们将重点关注胰岛β细胞死亡的主要机制和介质、辅助性T淋巴细胞对疾病进展的影响以及主要组织相容性复合体II类分子在赋予IDDM易感性方面的潜在作用。

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