Identifying the Cells Breaching Self-Tolerance in Autoimmunity
Identifying the Cells Breaching Self-Tolerance in Autoimmunity
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DOI：
10.4049/jimmunol.0903951
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发表时间：
2010-06-01
影响因子：
4.4
通讯作者：
Brewer, James M.
中科院分区：
文献类型：
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作者：
Benson, Robert A.;Patakas, Agapitos;Brewer, James M.
树突状细胞（DC）提呈自身抗原后，激活自身反应性T细胞被广泛认为是自身免疫性疾病发展的促发因素。然而，尽管有这样广泛的先入之见，支持数据是稀缺的和主观的，特别是在实验性关节病。我们已经采用了一种新的小鼠模型的破坏自身耐受性，允许评估的贡献内源性树突状细胞的自身免疫反应和疾病的发展。这是第一次，我们揭示了传统的DC所发挥的关键作用，以及这一过程的时间和位置。我们进一步证明了这一发现的重要性，通过临床相关的，常规的DC功能的治疗操作，导致降低自身免疫表型和疾病的严重程度。免疫学杂志，2010，184：6378-6385。
Activation of auto-reactive T cells by activated dendritic cells (DCs) presenting self-Ag is widely assumed to be the precipitating event in the development of autoimmune disease. However, despite such widely held preconceptions, supporting data are scarce and subjective, particularly in experimental arthropathy. We have adapted a novel murine model of breach of self-tolerance allowing evaluation of the contribution of endogenous DCs to the development of autoimmune responses and disease. For the first time, we reveal the critical role played by conventional DCs, and the timing and location of this process. We further demonstrate the importance of this finding by clinically relevant, therapeutic manipulation of conventional DC function, resulting in decreased autoimmune phenotype and disease severity. The Journal of Immunology, 2010, 184: 6378-6385.