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Seiji Kawamoto, Ali Yalcindag, Dhafer Laouini, Scott Brodeur, Paul Bryce, Bao Lu, Alison A. Humbles, Hans Oettgen, Craig Gerard, Raif S. Geha
J Clin Invest. 2004;
114(3):399
doi:10.1172/JCI19082
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echanical injury to the skin results in activation of the complement component C3 and release of the anaphylatoxin C3a. C3a binds to a seven-transmembrane G protein–coupled receptor, C3aR. We used C3aR–/– mice to examine the role of C3a in a mouse model of allergic inflammation induced by epicutaneous sensitization with OVA. C3aR–/– mice exhibited an exaggerated Th2 response to epicutaneous but not to intraperitoneal sensitization with OVA, as evidenced by significantly elevated levels of serum OVA-specific IgG1 and significantly increased secretion of the Th2 cytokines IL-4, IL-5, and IL-10 by antigen-stimulated splenocytes. Presentation of OVA peptide by C3aR–/– APCs caused significantly more IL-4 and IL-5 secretion by T cells from OVA–T cell receptor (OVA-TCR) transgenic mice compared with presentation by WT APCs. C3a inhibited the ability of splenocytes, but not of highly purified T cells, to secrete Th2 cytokines in response to TCR ligation. This inhibition was mediated by IL-12 secreted by APCs in response to C3a. These results suggest that C3a-C3aR interactions inhibit the ability of APCs to drive Th2 cell differentiation in response to epicutaneously introduced antigen and may have important implications for allergic skin diseases.
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