Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA.
J Allergy Clin Immunol. 2011 Feb;127(2):351-4. doi: 10.1016/j.jaci.2010.11.033.
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.
越来越多的动物模型研究表明，T 细胞受体 (TCR) 信号的改变单独作用就可以导致初始 T 细胞极向分化为 T(H)2 细胞，并获得 T(H)2 效应功能，从而导致 T(H)2 相关疾病。这些观察结果与人类疾病有很大的相关性。具体来说，一些与特应性疾病相关的免疫缺陷可能由于 TCR 信号的异常而表现出特应性。因此，尝试确定 TCR 信号缺陷在常见特应性疾病发病机制中的作用非常重要。
