Amphiregulin is not essential for induction of contact hypersensitivity

Akiko Yagami, Naoki Kajiwara, Keisuke Oboki, Tatsukuni Ohno, Hideaki Morita, Susan W. Sunnarborg, Ko Okumura, Hideoki Ogawa, Hirohisa Saito, Susumu Nakae

研究成果: ジャーナルへの寄稿学術論文査読

4 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)277-284
ページ数8
ジャーナルAllergology International
59
3
DOI
出版ステータス出版済み - 2010
外部発表はい

All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学

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