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: Article

3 引用 (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.

元の言語English
ページ(範囲)277-284
ページ数8
ジャーナルAllergology International
59
発行部数3
DOI
出版物ステータスPublished - 01-01-2010
外部発表Yes

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Contact Dermatitis
Fluorescein
Dinitrofluorobenzene
Th2 Cells
Eosinophil Peroxidase
Cytokines
Peroxidase
Cell Movement
Ear
Immunoglobulins
Lymph Nodes
Enzyme-Linked Immunosorbent Assay
Cell Proliferation
isothiocyanic acid
Amphiregulin
Th1 Cells
Langerhans Cells
Serum
Dendritic Cells
Thymidine

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy

これを引用

Yagami, A., Kajiwara, N., Oboki, K., Ohno, T., Morita, H., Sunnarborg, S. W., ... Nakae, S. (2010). Amphiregulin is not essential for induction of contact hypersensitivity. Allergology International, 59(3), 277-284. https://doi.org/10.2332/allergolint.09-OA-0149
Yagami, Akiko ; Kajiwara, Naoki ; Oboki, Keisuke ; Ohno, Tatsukuni ; Morita, Hideaki ; Sunnarborg, Susan W. ; Okumura, Ko ; Ogawa, Hideoki ; Saito, Hirohisa ; Nakae, Susumu. / Amphiregulin is not essential for induction of contact hypersensitivity. :: Allergology International. 2010 ; 巻 59, 番号 3. pp. 277-284.
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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 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.",
author = "Akiko Yagami and Naoki Kajiwara and Keisuke Oboki and Tatsukuni Ohno and Hideaki Morita and Sunnarborg, {Susan W.} and Ko Okumura and Hideoki Ogawa and Hirohisa Saito and Susumu Nakae",
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Yagami, A, Kajiwara, N, Oboki, K, Ohno, T, Morita, H, Sunnarborg, SW, Okumura, K, Ogawa, H, Saito, H & Nakae, S 2010, 'Amphiregulin is not essential for induction of contact hypersensitivity', Allergology International, 巻. 59, 番号 3, pp. 277-284. https://doi.org/10.2332/allergolint.09-OA-0149

Amphiregulin is not essential for induction of contact hypersensitivity. / Yagami, Akiko; Kajiwara, Naoki; Oboki, Keisuke; Ohno, Tatsukuni; Morita, Hideaki; Sunnarborg, Susan W.; Okumura, Ko; Ogawa, Hideoki; Saito, Hirohisa; Nakae, Susumu.

:: Allergology International, 巻 59, 番号 3, 01.01.2010, p. 277-284.

研究成果: Article

TY - JOUR

T1 - Amphiregulin is not essential for induction of contact hypersensitivity

AU - Yagami, Akiko

AU - Kajiwara, Naoki

AU - Oboki, Keisuke

AU - Ohno, Tatsukuni

AU - Morita, Hideaki

AU - Sunnarborg, Susan W.

AU - Okumura, Ko

AU - Ogawa, Hideoki

AU - Saito, Hirohisa

AU - Nakae, Susumu

PY - 2010/1/1

Y1 - 2010/1/1

N2 - 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.

AB - 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.

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DO - 10.2332/allergolint.09-OA-0149

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JO - Allergology International

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SN - 1323-8930

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