Humoral Autoimmunity in Type 1 Diabetes: Prediction, Significance, and Detection of Distinct Disease Subtypes

被引:51
|
作者
Pietropaolo, Massimo [1 ]
Towns, Roberto [1 ]
Eisenbarth, George S. [2 ]
机构
[1] Univ Michigan, Sch Med, Dept Internal Med, Brehm Ctr Diabet Res,Lab Immunogenet, Ann Arbor, MI 48105 USA
[2] Univ Colorado Denver, Barbara Davis Ctr Childhood Diabet, Aurora, CO 80045 USA
来源
基金
美国国家卫生研究院;
关键词
GLUTAMIC-ACID DECARBOXYLASE; PROTEIN-TYROSINE-PHOSPHATASE; B-LYMPHOCYTE DEPLETION; ISLET-CELL ANTIBODIES; CD4(+) T-CELLS; HIGH-RISK; RHEUMATOID-ARTHRITIS; INSULIN AUTOANTIBODY; PREDIABETIC PROCESS; MOLECULAR-CLONING;
D O I
10.1101/cshperspect.a012831
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Type 1 diabetes mellitus (T1D) is an autoimmune disease encompassing the T-cell-mediated destruction of pancreatic beta cells and the production of autoantibodies against islet proteins. In humoral autoimmunity in T1D, the detection of islet autoantibodies and the examination of their associations with genetic factors and cellular autoimmunity constitute major areas in both basic research and clinical practice. Although insulin is a key autoantigen and may be primus inter pares in importance among T1D autoantigens, an abundant body of research has also revealed other autoantigens associated with the disease process. Solid evidence indicates that autoantibodies against islet targets serve as key markers to enroll newly diagnosed T1D patients and their family members in intervention trials aimed at preventing or halting the disease process. The next challenge is perfecting mechanistic bioassays to be used as end points for disease amelioration following immunomodulatory therapies aimed at blocking immune-mediated beta-cell injury and, in turn, preserving beta-cell function in type 1 diabetes mellitus.
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页数:18
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