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J Dermatol Sci. 2004 Oct;36(1):51-6.

Hapten-induced contact hypersensitivity is enhanced in Tyk2-deficient mice.

Author information

1
Biochemistry Laboratory, Pias Corporation, 1-3-1 Murotani, Nishi-ku, Kobe 651-2241, Japan. miwahoso@kuhp.kyoto-u.ac.jp

Abstract

BACKGROUND:

Previous studies have shown that Tyk2, a member of the Janus family of protein tyrosine kinases, which are activated by a variety of cytokines, plays a crucial role in interleukin (IL)-12-mediated T-cell functions such as IFN-gamma production. On the other hand, hapten-induced contact hypersensitivity (CHS) is mediated by IFN-gamma producing CD8+ T cells and regulated by CD4+ T cells.

OBJECTIVE:

This study hypothesized that the CHS response might be reduced in Tyk2-deficient mice because of a lack of IFN-gamma production from CD4+ and CD8+ T cells.

METHODS:

The CHS reaction was evoked in wild-type and Tyk2-deficient mice and the ears of the mice were examined to measure for several cytokines.

RESULTS:

Ear swelling during CHS was significantly enhanced in Tyk2-deficient mice compared with the controls. IL-12 and IFN-gamma levels at the reaction sites in Tyk2-deficient mice were significantly lower than in the controls, whereas IL-2 and IL-4 levels were elevated. Furthermore, STAT3- and STAT4-phosphorylation in the draining lymph node cells of Tyk2-deficient mice decreased.

CONCLUSION:

These results suggest that the lack of Tyk2-mediated signal transduction enhances a compensative pathway during CHS.

PMID:
15488705
DOI:
10.1016/j.jdermsci.2004.07.007
[Indexed for MEDLINE]

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