NDLI: CXCR3 deficiency prolongs Th1-type contact hypersensitivity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Miyagaki, Tomomitsu Sugaya, Makoto Okochi, Hitoshi Sato, Shinichi Ohmatsu, Hanako Suga, Hiraku
Description	Country affiliation: Japan Author Affiliation: Suga H ( Department of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo 113-8655, Japan.)
Abstract	Sensitization and challenge using dinitrofluorobenzene (DNFB) induce contact hypersensitivity (CHS) with Th1 cell infiltration, whereas those using FITC generate CHS with Th2 cell infiltration. In this study, we attempted to determine the role of CXCR3, a chemokine receptor, in Th1- and Th2-type CHS induced by DNFB or FITC using CXCR3-deficient (CXCR3(-/-)) mice. Ear swelling was prolonged after DNFB challenge in CXCR3(-/-) mice, which was accompanied by increased Th1 cytokines and decreased TGF-ß and IL-10 expression at a late time point of CHS, whereas there was no significant difference between wild-type and CXCR3(-/-) mice in FITC-induced CHS. In Th1-type CHS, the number of regulatory T cells (Tregs) was decreased in the challenged ear of CXCR3(-/-) mice compared with that of wild-type mice, suggesting that CXCR3 would be important in migration of Tregs into the site of inflammation. Moreover, we examined the characteristics of CXCR3(+) Tregs both in vitro and in vivo, revealing that CXCR3(+) Tregs expressed high levels of TGF-ß and IL-10 as well as IFN-Î³ compared with CXCR3(-) Tregs. When CXCR3(-/-) mice were injected with CXCR3(+) Tregs, the prolonged ear swelling induced by DNFB was normalized. Taken together, our results suggest that CXCR3(+) Tregs play a key role for quenching Th1-type CHS.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dermatitis, Contact Immunology Receptors, Cxcr3 Th1 Cells Adoptive Transfer Animals Dinitrofluorobenzene Fluorescein-5-isothiocyanate Toxicity Fluorescent Antibody Technique Immunohistochemistry Irritants Mice Mice, Inbred C57bl Mice, Knockout Deficiency Reverse Transcriptase Polymerase Chain Reaction Th2 Cells Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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