Amphiregulin 对于诱导接触性过敏反应不是必需的。

Amphiregulin is not essential for induction of contact hypersensitivity.

机构信息

Department of Allergy and Immunology, National Research Institute for Child Health and Development.

Department of Allergy and Immunology, National Research Institute for Child Health and Development,; Atopy Research Center, Juntendo University.

出版信息

Allergol Int. 2010 Sep;59(3):277-284. doi: 10.2332/allergolint.09-OA-0149. Epub 2010 Jun 25.

DOI:10.2332/allergolint.09-OA-0149

PMID:20567134

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.

摘要

背景

Amphiregulin (AR) 在 Th2 细胞中表达，而不是 Th1 细胞，在 Th2 细胞/细胞因子介导的宿主防御针对线虫的过程中发挥重要作用。我们之前还发现，在 Th2 细胞/细胞因子介导的荧光素异硫氰酸酯（FITC）诱导的接触超敏反应（CHS）中，炎症组织中 AR mRNA 的表达被强烈上调，这表明 AR 有助于诱导这些反应。

方法

为了阐明 AR 在 FITC 或二硝基氟苯（DNFB）诱导的 CHS 诱导中的作用，用 FITC 或 DNFB 经皮致敏和/或挑战 AR 缺陷型小鼠。通过流式细胞术评估 FITC 介导的皮肤树突状细胞（DC）迁移和 FITC 特异性淋巴结细胞增殖和细胞因子产生的水平，分别通过[3H]胸腺嘧啶掺入和 ELISA 评估 FITC 致敏后的 FITC 特异性淋巴节点细胞增殖和细胞因子产生的水平。通过组织学分析、比色测定和 ELISA 分别评估耳肿胀程度、炎症部位髓过氧化物酶（MPO）和嗜酸性粒细胞过氧化物酶（EPO）的活性以及血清中 FITC 特异性免疫球蛋白（Ig）的水平，在 FITC 挑战后。