John Libbey Eurotext

European Journal of Dermatology


Co-existence of specific IgE antibodies and T cells reactive to house dust mites and human transglutaminase3/tropomysin in patients with atopic dermatitis Article à paraître


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1 Department of Dermatology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health. 56 South Lishi Road, Xicheng District, Beijing 100045, China
2 Department of Dermatology, Peking University People's Hospital, No. 11 Xizhimen South St., Beijing 100044, China
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Background: Although specific IgE antibodies reactive to exogenous antigens are found in patients with atopic dermatitis (AD), some patients do not have such antibodies. Autoimmunity has been proposed as a possible mechanism in these patients. Objectives: To identify specific IgE antibodies reactive to human transglutaminase 3 (TG3) and tropomysin (TMP) and determine whether auto-reactive T cells are induced by these proteins in patients with AD. Materials & Methods: Forty-two patients with AD and 27 healthy controls were included in this study. IgE antibodies against recombinant human TG3 and TMP were measured by ELISA. Cross-reactivity between allergens was determined by EdU of peripheral blood mononuclear cells (PBMCs) proliferation assays. T-cell lines were generated from PBMCs in the presence of house dust mites (HDM), TG3 and TMP. TG3/TP–specific T-cell clones were generated from T-cell lines, and were characterized by antigen specificity and cytokine pattern. Results: In 12 patients with anti-HDM IgE antibodies, six (50%) had anti-TG3 IgE antibody and four (33.3%) had both anti-TG3 and anti-TMP IgE antibodies. Lymphocyte proliferation was induced in 12 patients by TG3 or TMP. T-cell lines and T-cell clones from PBMCs of patients with AD who had IgE antibody reactive to HDM were fully cross-reactive with TG3 and TMP. These cell clones included both Th1 cell (producing IFN-γ) and Th2 cell (inducing IL-4) responses. TG3–and TMP–specific T-cell clones were not generated from healthy controls. Conclusion: Specific IgE antibody and T cell clones reactive to human TG3 and TMP were found in patients with AD, indicating that an autoimmune mechanism might contribute to AD.