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Allergy Asthma Immunol Res. 2013 Jul;5:e179. English.
Published online 2013 July 02. |
| Copyright © 2013 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease |
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Toshiaki Kawakami, 1,2 Jun-ichi Kashiwakura,2 and Yuko Kawakami1 |
| 1Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, California, USA. |
| 2Laboratory of Allergic Disease, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), Yokohama, Kanagawa, Japan. |
Correspondence to: Toshiaki Kawakami, MD, PhD, Division of Cell Biology, La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, California 92037-1387, USA. Tel: +1-858-752-6814; Fax: +1-858-752-6986; Email: toshi@liai.org
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Received November 02, 2012; Revised December 27, 2012; Accepted January 15, 2013.
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Abstract
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Factors that can induce the release of histamine from basophils have been studied for more than 30 years. A protein termed histamine-releasing factor (HRF) was purified and molecularly cloned in 1995. HRF can stimulate histamine release and IL-4 and IL-13 production from IgE-sensitized basophils and mast cells. HRF-like activities were found in bodily fluids during the late phase of allergic reactions, implicating HRF in allergic diseases. However, definitive evidence for the role of HRF in allergic diseases has remained elusive. On the other hand, we found effects of monomeric IgE on the survival and activation of mast cells without the involvement of a specific antigen, as well as heterogeneity of IgEs in their ability to cause such effects. The latter property of IgE molecules seemed to be similar to the heterogeneity of IgEs in their ability to prime basophils in response to HRF. This similarity led to our recent finding that ~30% of IgE molecules can bind to HRF via their Fab interactions with two binding sites within the HRF molecule. The use of peptide inhibitors that block HRF-IgE interactions revealed an essential role of HRF to promote skin hypersensitivity and airway inflammation. This review summarizes this and more recent findings and provides a perspective on how they impact our understanding of allergy pathogenesis and potentially change the treatment of allergic diseases.
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Keywords: Asthma, allergy, histamine-releasing factor, IgE, mast cell, basophil.
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Open Access
Article
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