Altered T-cell receptor signaling in the pathogenesis of allergic disease

被引:13
作者
Datta, Shrimati [1 ]
Milner, Joshua D. [1 ]
机构
[1] NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA
基金
美国国家卫生研究院;
关键词
T-cell receptor; T(H)2; atopy; IMMUNOLOGICAL SYNAPSE; AUTOIMMUNE ARTHRITIS; DOCK8; MUTATIONS; OMENN-SYNDROME; CUTTING EDGE; ACTIVATION; MICE; RESPONSES; KINASE; IMMUNODEFICIENCY;
D O I
10.1016/j.jaci.2010.11.033
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Mounting evidence from animal models has demonstrated that alterations in T-cell receptor (TCR) signaling alone can lead to dramatically skewed differentiation of naive T cells into T(H)2 cells, to T(H)2 effector functions, and to T(H)2-related diseases. There is significant potential relevance of these observations to human disease. Specifically, a number of immunodeficiencies associated with atopic disease might have atopy as a manifestation because of aberrant TCR signaling. It is therefore important to attempt to identify a role for defects in TCR signaling in the pathogenesis of common atopic diseases. (J Allergy Clin Immunol 2011;127:351-4.)
引用
收藏
页码:351 / 354
页数:4
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