Please use this identifier to cite or link to this item:
Title: An essential role for IL-18 in CD8 T cell-mediated suppression of IgE responses
Authors: Salagianni, M.
Loon, W.K.
Thomas, M.J.
Noble, A.
Kemeny, D.M. 
Issue Date: 15-Apr-2007
Citation: Salagianni, M.,Loon, W.K.,Thomas, M.J.,Noble, A.,Kemeny, D.M. (2007-04-15). An essential role for IL-18 in CD8 T cell-mediated suppression of IgE responses. Journal of Immunology 178 (8) : 4771-4778. ScholarBank@NUS Repository.
Abstract: The ability of CD8 T cells to suppress IgE responses is well established. Previously, we demonstrated that CD8 T cells inhibit IgE responses via the induction of IL-12, which promotes Th1 and suppresses Th2 responses. In this study, we show that IL-18 also plays an essential role in IgE suppression. In vitro, IL-18 synergized with IL-12 to promote Th1/T cytotoxic 1 and inhibit Th2/T cytotoxic 2 differentiation. OVA-specific TCR transgenic (OT-I) CD8 cells induced both IL-12 and IL-18 when cultured with OVA257-264 peptide-pulsed dendritic cells. In vivo, IL-18-/- mice exhibited higher IgE and IgG1 levels compared with wild-type mice after immunization with OVA/alum. Furthermore, adoptive transfer of CD8 T cells from OVA-primed mice suppressed IgE responses in OVA/alum-immunized mice, but not in IL-18 -/- mice. IgE suppression in IL-18-/- mice was restored if CD8 T cells were coadoptively transferred with IL-18-competent wild-type bone marrow dendritic cell progenitors, demonstrating an essential role of IL-18 in CD8 T cell-mediated suppression of IgE responses. The data suggest that CD8 T cells induce IL-18 production during a cognate interaction with APCs that synergizes with IL-12 to promote immune deviation away from the allergic phenotype. Our data identify IL-18 induction as a potentially useful target in immunotherapy of allergic disease. Copyright © 2007 by The American Association of Immunologists, Inc.
Source Title: Journal of Immunology
ISSN: 00221767
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

Google ScholarTM


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.