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Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL 35294
Allergen-induced contact hypersensitivity (CHS) is a T cell-mediated delayed-type immune response which has been considered to be primarily mediated by CD8+ T cytotoxic type I (Tc1) cells. IFN-
, the prototype Tc1 (Th1) cytokine, has been implicated as the primary inflammatory cytokine for CHS. In this study, we demonstrate that neutralization of IL-17 rather than IFN- suppresses the elicitation of CHS. The suppression does not result from inhibition of the proliferation of allergen-activated T cells. Allergen sensitization induces the development of distinct CD8+ T cell subpopulations that produce IFN- or IL-17. Although CD8+ IL-17-producing cells are stimulated by IL-23, they are inhibited by IL-12, a prototypical stimulator of IFN--producing Tc1 cells. This indicates that CD8+ IL-17-producing cells are distinct from Tc1 cells and are important in effector functions at the elicitation of CHS. These studies provide insights into a novel mechanism for CHS.
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 Grant Number AR46256 from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (to. H.X). This investigation was conducted in a facility constructed with support from Research Facilities Improvement Program Grant No. C06 RR 15490 from the National Center for Research Resources, National Institutes of Health.
2 Address correspondence and reprint requests to Dr. Hui Xu, Department of Dermatology, University of Alabama at Birmingham, VH566B, 1670 University Boulevard, Birmingham, AL 35294. E-mail address: xuhui{at}uab.edu
3 Abbreviations used in this paper: CHS, contact hypersensitivity; Tc1, T cytotoxic type I; DNFB, dinitrofluorobenzene; DNBS, dinitrobenzenesulfonic acid, sodium salt; DC, dendritic cell; BM-DC, bone marrow-derived DC.
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