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
Department of Dermatology, Peking University People's Hospital, No. 11 Xizhimen South St., Beijing 100044, China
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.