T cell homing to epithelial barriers in allergic disease

被引:172
作者
Islam, Sabina A. [1 ]
Luster, Andrew D. [1 ]
机构
[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Immunol & Inflammatory Dis,Div Rheumatol Alle, Boston, MA 02115 USA
基金
美国国家卫生研究院;
关键词
CHEMOKINE RECEPTORS CCR4; ACTIVATION-REGULATED CHEMOKINE; CUTANEOUS LYMPHOCYTE ANTIGEN; ATOPIC-DERMATITIS; DENDRITIC CELLS; MOUSE MODEL; CUTTING EDGE; DIFFERENTIAL EXPRESSION; AIRWAY INFLAMMATION; CYTOKINE PRODUCTION;
D O I
10.1038/nm.2760
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Allergic inflammation develops in tissues that have large epithelial surface areas that are exposed to the environment, such as the lung, skin and gut. In the steady state, antigen-experienced memory T cells patrol these peripheral tissues to facilitate swift immune responses against invading pathogens. In at least two allergy-prone organs, the skin and the gut, memory T cells are programmed during the initial antigen priming to express trafficking receptors that enable them to preferentially home to these organs. In this review we propose that tissue-specific memory and inflammation-specific T cell trafficking facilitates the development of allergic disease in these organs. We thus review recent advances in our understanding of tissue-specific T cell trafficking and how regulation of T cell trafficking by the chemokine system contributes to allergic inflammation in mouse models and in human allergic diseases of the skin, lung and gut. Inflammation-and tissue-specific T lymphocyte trafficking pathways are currently being targeted as new treatments for non-allergic inflammatory diseases and may yield effective new therapeutics for allergic diseases.
引用
收藏
页码:705 / 715
页数:11
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