CCR3 is required for tissue eosinophilia and larval cytotoxicity after infection with Trichinella spiralis

被引:72
作者
Gurish, MF
Humbles, A
Tao, H
Finkelstein, S
Boyce, JA
Gerard, C
Friend, DS
Austen, KF
机构
[1] Brigham & Womens Hosp, Dept Med, Div Rheumatol Allergy & Immunol, Boston, MA 02115 USA
[2] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA
[4] Beth Israel Hosp, Dept Pediat, Boston, MA 02115 USA
[5] Childrens Hosp, Dept Pediat, Boston, MA 02115 USA
关键词
D O I
10.4049/jimmunol.168.11.5730
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The CCR3 binds at least seven different CC chemokines and is expressed on eosinophils, mast cells (MC), and a subset of Th cells (Th2) that generate cytokines implicated in mucosal immune responses. Using mice with a targeted disruption of CCR3 (CCR3(-/-)) and their +/+ littermates, we investigated the role of CCR3 in the amplification of tissue eosinophilia and MC hyperplasia in the mouse after infection with Trichinella spiralis. In CCR3-/- mice, eosinophils are not recruited to the jejunal mucosa after infection and are not present in the skeletal muscle adjacent to encysting larvae. In addition, the number of cysts in the skeletal muscle is increased and the frequency of encysted larvae exhibiting necrosis is reduced. The CCR3(-/-) mice exhibit the expected MC hyperplasia in the jejunum and caecum and reject the adult worms from the small intestine at a normal rate. This study is consistent with distinct functions for MC (adult worm expulsion) and eosinophils (toxicity to larvae) in immunity to a helminth, T. spiralis, and defines the essential requirement for CCR3 in eosinophil, but not MC recruitment to tissues.
引用
收藏
页码:5730 / 5736
页数:7
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