2010年
Amphiregulin is not essential for induction of contact hypersensitivity
Allergology International
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- 巻
- 59
- 号
- 3
- 開始ページ
- 277
- 終了ページ
- 284
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.2332/allergolint.09-OA-0149
- 出版者・発行元
- Japanese Society of Allergology
Background: Amphiregulin (AR) is expressed in Th2 cells, rather than Th1 cells, and plays an important role in Th2 cell/cytokine-mediated host defense against nematodes. We also found earlier that AR mRNA expression was strongly upregulated in inflamed tissue during Th2 cell/cytokine-mediated fluorescein isothiocyanate (FITC)-induced contact hypersensitivity (CHS), suggesting a contribution of AR to the induction of those responses. Methods: To elucidate the role of AR in the induction of FITC- or dinitrofluorobenzene (DNFB)-induced CHS, AR-deficient mice were sensitized and/or challenged with FITC or DNFB epicutaneously. The levels of FITCmediated skin dendritic cell (DC) migration and FITC-specific lymph node cell proliferation and cytokine production were assessed by flow cytometry, [3H]-thymidine incorporation and ELISA, respectively, after FITC sensitization. The degree of ear swelling, the activities of myeloperoxidase (MPO) and eosinophil peroxidase (EPO) in inflammatory sites and the levels of FITC-specific immunoglobulin (Ig) in sera were determined by histological analysis, colorimetric assay and ELISA, respectively, after FITC challenge. Results: DC migration and FITC-specific lymph node cell proliferation and cytokine production were normal in the AR-deficient mice. Ear swelling, tissue MPO and EPO activities and FITC-specific serum Ig levels were also similar in AR-deficient and -sufficient mice. Conclusions: Amphiregulin is not essential for the induction of FITC- or DNFB-induced CHS responses in mice. © 2010 Japanese Society of Allergology.
- ID情報
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- DOI : 10.2332/allergolint.09-OA-0149
- ISSN : 1440-1592
- ISSN : 1323-8930
- SCOPUS ID : 77957242913