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International Immunology Advance Access originally published online on January 15, 2009
International Immunology 2009 21(2):187-201; doi:10.1093/intimm/dxn137
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© The Japanese Society for Immunology. 2009. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Ablation of type I hypersensitivity in experimental allergic conjunctivitis by eotaxin-1/CCR3 blockade

Dai Miyazaki1, Takao Nakamura2, Masaharu Ohbayashi2, Chuan Hui Kuo1, Naoki Komatsu1, Keiko Yakura1, Takeshi Tominaga1, Yoshitsugu Inoue1, Hidemitsu Higashi3, Meguru Murata3, Shuzo Takeda3, Atsuki Fukushima4, Fu-Tong Liu5, Marc E. Rothenberg6 and Santa Jeremy Ono2

1 Division of Ophthalmology and Visual Science, Tottori University Faculty of Medicine, Tottori, Japan
2 Emory University School of Medicine and Emory Eye Center, Dobbs Ocular Immunology Laboratories, Atlanta, GA 30338, USA
3 Pharmaceuticals Research Division, Mitsubishi Tanabe Pharma Co., Yokohama, Japan
4 Department of Ophthalmology, Kochi Medical School, Kohasu, Oko-cho, Nankoku-city, Japan
5 Department of Dermatology, University of California, Davis, School of Medicine, Sacramento, CA 95816, USA
6 Division of Allergy and Immunology, Department of Pediatrics, University of Cincinnati College of Medicine, Children's Hospital Medical Center, Cincinnati, OH 45229, USA

Correspondence to: D. Miyazaki; E-mail: dm{at}grape.med.tottori-u.ac.jp

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.

Keywords: mast cell

Transmitting editor: S. Koyasu

Received 14 September 2008, accepted 4 December 2008.


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T. Tominaga, D. Miyazaki, S.-i. Sasaki, S. Mihara, N. Komatsu, K. Yakura, and Y. Inoue
Blocking Mast Cell-Mediated Type I Hypersensitivity in Experimental Allergic Conjunctivitis by Monocyte Chemoattractant Protein-1/CCR2
Invest. Ophthalmol. Vis. Sci., November 1, 2009; 50(11): 5181 - 5188.
[Abstract] [Full Text] [PDF]


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