Allergology International (Jan 2010)

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

Journal volume & issue
Vol. 59, no. 3
pp. 277 – 284

Abstract

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ABSTRACT: 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 FITC- mediated 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. KEY WORDS: amphiregulin, contact dermatitis, EGF, mast cells, Th2 cell/cytokine