The role of CCR7 in allergic airway inflammation induced by house dust mite exposure

被引:23
作者
Kawakami, Masaki [1 ,2 ]
Narumoto, Osamu [1 ,2 ]
Matsuo, Yukiko [1 ]
Horiguchi, Kazuhide [3 ]
Horiguchi, Satomi [3 ]
Yamashita, Naohide [4 ]
Sakaguchi, Masahiro [5 ]
Lipp, Martin [6 ]
Nagase, Takahide [2 ]
Yamashita, Naomi [1 ]
机构
[1] Musashino Univ, Pharmaceut Sci Res Inst, Dept Pharmacotherapy, Nishitokyo, Tokyo 2028585, Japan
[2] Univ Tokyo, Fac Med, Dept Pulm Med, Tokyo 113, Japan
[3] Univ Fukui, Fac Med Sci, Dept Anat, Fukui 910, Japan
[4] Univ Tokyo, Inst Med Sci, Dept Adv Med Sci, Tokyo, Japan
[5] Azabu Univ, Sch Vet Med, Dept Vet Microbiol, Sagamihara, Kanagawa, Japan
[6] Max Delbruck Ctr Mol Med, Berlin, Germany
关键词
Asthma; Airway hyperresponsiveness; CCR7; CCL21; House dust mite; Airway inflammation; REGULATORY T-CELLS; SECONDARY LYMPHOID ORGANS; RECEPTOR; 4; PERIPHERAL-TISSUES; IMMUNE-RESPONSES; DENDRITIC CELLS; ASTHMA MODEL; TGF-BETA; MIGRATION; HMGB1;
D O I
10.1016/j.cellimm.2012.03.009
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
House dust mite (HDM), the most common allergen, activate both the IgE-associated and innate immune responses. To clarify the process of sensitization, we investigated the role of the CCL21, CCL19, and CCR7 axis in a mouse model of HDM-induced allergic asthma. HDM inhalation without systemic immunization resulted in a HDM-specific IgE response. CCR7-knockout (CCR7KO) mice exhibited greater airway inflammation and IgE responses compared to wild-type mice. We examined FoxP3 expression in these mice to clarify the contribution of regulatory cells to the responses. FoxP3 expression was higher in the lungs but not in the lymph nodes of CCR7KO mice compared to wild-type mice. In CCR7KO mice, FoxP3-positive cells were found in lung, but we observed higher release of IL-13, IL-5, TGF-beta, IL-17, and HMGB1 in bronchoalveolar lavage fluid. We demonstrate here that immuno-regulation through CCR7 expression in T cells plays a role in HDM-specific sensitization in the airway. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:24 / 32
页数:9
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