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- Title
Ablation of type I hypersensitivity in experimental allergic conjunctivitis by eotaxin-1/CCR3 blockade.
- Authors
Dai Miyazaki; Takao Nakamura; Masaharu Ohbayashi; Chuan Hui Kuo; Naoki Komatsu; Keiko Yakura; Takeshi Tominaga; Yoshitsugu Inoue; Hidemitsu Higashi; Meguru Murata; Shuzo Takeda; Atsuki Fukushima; Fu-Tong Liu; Marc E. Rothenberg; Santa Jeremy Ono
- Abstract
The immune response is regulated, in part, by effector cells whose activation requires multiple signals. For example, T cells require signals emanating from the T cell antigen receptor and co-stimulatory molecules for full activation. Here, we present evidence indicating that IgE-mediated hypersensitivity reactions in vivo also require cognate signals to activate mast cells. Immediate hypersensitivity reactions in the conjunctiva are ablated in mice deficient in eotaxin-1, despite normal numbers of tissue mast cells and levels of IgE. To further define the co-stimulatory signals mediated by chemokine receptor 3 (CCR3), an eotaxin-1 receptor, effects of CCR3 blockade were tested with an allergic conjunctivitis model and in ex vivo isolated connective tissue-type mast cells. Our results show that CCR3 blockade significantly suppresses allergen-mediated hypersensitivity reactions as well as IgE-mediated mast cell degranulation. We propose that a co-stimulatory axis by CCR3, mainly stimulated by eotaxin-1, is pivotal in mast cell-mediated hypersensitivity reactions.
- Subjects
MAST cells; BASOPHILS; CONNECTIVE tissue cells; IMMUNOGLOBULIN E; T cells; ADNEXA oculi
- Publication
International Immunology, 2009, Vol 21, Issue 2, p187
- ISSN
0953-8178
- Publication type
Article
- DOI
10.1093/intimm/dxn137