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-Chain on APCs in the Development of Allergen-Induced Airway Hyperresponsiveness and Inflammation1
* Department of Medicine II, Faculty of Medicine, Okayama University Medical School, Okayama, Japan;
Department of Pediatrics, Division of Cell Biology, National Jewish Medical and Research Center, Denver, CO; and
Department of Experimental Immunology and Core Research for Evolutional Science and Technology Program, Japan Science and Technology Agency, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan
The FcR common 
-chain (FcR) is an essential component of the receptors Fc
RI, FcRI, and FcRIII, which are expressed on many inflammatory cell types. The role of these receptors in the initiation or maintenance of allergic inflammation has not been well defined. FcR-deficient (FcR–/–) and control (wild-type (WT)) mice were sensitized and subsequently challenged with OVA. Following sensitization and challenge to OVA, FcR-deficient (FcR–/–) mice developed comparable levels of IgE and IgG1 as WT mice. However, numbers of eosinophils, levels of IL-5, IL-13, and eotaxin in bronchoalveolar lavage fluid, and mononuclear cell (MNC) proliferative responses to OVA were significantly reduced, as was airway hyperresponsiveness (AHR) to inhaled methacholine. Reconstitution of FcR–/– mice with whole spleen MNC from WT mice before sensitization restored development of AHR and the numbers of eosinophils in bronchoalveolar lavage fluid; reconstitution after sensitization but before OVA challenge only partially restored these responses. These responses were also restored when FcR–/– mice received T cell-depleted MNC, T and B cell-depleted MNC, or bone marrow-derived dendritic cells before sensitization from FcR+/+ or FcRIII-deficient but not FcR–/– mice. The expression levels of FcRIV on bone marrow-derived dendritic cells from FcR+/+ mice were found to be low. These results demonstrate that expression of FcR, most likely FcRI, on APCs is important during the sensitization phase for the development of allergic airway inflammation and AHR.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grants HL-36577 and HL-61005 and Environmental Protection Agency Grant R825702.
2 K.K. and K.T. contributed equally to this study.
3 The laboratories of E.W.G. and M.H. contributed equally to this study.
4 Address correspondence and reprint requests to Dr. Erwin W. Gelfand, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206. E-mail address: gelfande{at}njc.org
5 Abbreviations used in this paper: DC, dendritic cell; AHR, airway hyperresponsiveness; WT, wild type; BAL, bronchoalveolar lavage; PBLN, peribronchial lymph node; MNC, mononuclear cell; PAS, periodic acid-Schiff; MBP, major basic protein; MCh, methacholine; RL, lung resistance; BM-DC, bone marrow-derived DC.
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  C. von Garnier, M. E. Wikstrom, G. Zosky, D. J. Turner, P. D. Sly, M. Smith, J. A. Thomas, S. R. Judd, D. H. Strickland, P. G. Holt, et al. Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa J. Immunol., November 1, 2007; 179(9): 5748 - 5759. [Abstract] [Full Text] [PDF]
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