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International Immunology Advance Access published online on March 29, 2004
International Immunology, doi:10.1093/intimm/dxh073
© 2004 by The Japanese Society for Immunology
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Received December 1, 2003
Accepted February 4, 2004

Article

Essential role of MHC II-independent CD4+ T cells, IL-4 and STAT6 in contact hypersensitivity induced by fluorescein isothiocyanate in the mouse

Keisuke Takeshita 1, Tsugiko Yamasaki 1, Shizuo Akira 1, Florian Gantner 1, Kevin B. Bacon 1*

1 Bayer Yakuhin, Ltd., Research Center Kyoto, Department of Respiratory Diseases Research, Japan

* To whom correspondence should be addressed. E-mail: kevin.bacon.kb{at}bayer.co.jp.


  Abstract

Contact hypersensitivity (CHS) induced by a hapten is thought to be mediated by T helper type 1 (Th1) cells. However, FITC can induce contact allergy in vivo, and in vitro studies suggest that this response is Th2-type driven. We compared CHS reactions induced by FITC or dinitrofluorobenzene (DNFB), a well-known Th1 inducing hapten, in Balb/c mice, C57/B6 mice, and several gene knock-out mice, and investigated the role of Th1/Th2 cytokines, T cell populations, eosinophils, and mast cells. Balb/c mice (Th2 dominant strain) had a stronger response to FITC than C57/B6 mice (Th1 dominant strain). The skin inflammation was characterized by edema and eosinophilia, and serum IgE levels were elevated following FITC challenge. All responses were enhanced by a second round of sensitization. Anti-TNF-{alpha} or anti-very late antigen-4 (VLA-4) antibody partly inhibited both FITC- and DNFB-induced CHS. Pretreatment of mice with anti-IL-4 antibody, anti-IL-5 antibody, recombinant INF-{gamma}, or the mast-cell depleting agent 48/80 significantly diminished edema formation, and Stat6-/- mice were fully protected from FITC-induced CHS, while DNFB-induced CHS was enhanced (Stat6-/-, mast cell depletion) or not affected (anti-IL-5 antibody). Further, mice lacking CD4+ T cells and mice lacking both CD8 and MHC II showed very little reaction at all to FITC, while the absence of CD8 T cells alone or MHC II alone conferred partial protection only. These findings indicate a contribution of MHC II-independent CD4+ T cells and/or CD4+ NKT cells to the Th2 response triggered by FITC in vivo, and makes FITC-induced CHS a suitable animal model for atopic dermatitis.

Keywords: Keywords: allergy, eosinophils, mast cells, skin, Th1/2 cells


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