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Purpose: Cutaneous lymphocyte-associated antigen (CLA)-expressing CD8+T cells have been known to play an important role in the pathogenesis of atopic dermatitis(AD). However, the mechanisms underlying the loss of self-tolerance remainunclear. Regulatory T cells (Tregs) play a key role in the development of homeostasisin the immune system. We, therefore, hypothesized that a reduced ability of Tregs to inhibit autologous CD8+CLA+T cells might be underlying mechanism in AD. Materials and Methods: CD8+CLA+T cells and Tregs were obtained from the peripheral blood of AD patients and control volunteers. The frequenciesof CD8+CLA+T cells were evaluated. The proliferative responses of CD8+CLA+T cells were assessed by flow cytometry, and the levels of transforming growth factor-β1 (TGF-β1) and interleukin-10 (IL-10) in culture supernatants were detected by enzyme-linked immunosorbent assay. Results: Our results revealed higher frequency and increased expression of perforin and granzyme-B in peripheralCD8+CLA+T cells in AD, and lower inhibitory ability of Tregs on proliferation of CD8+CLA+T cells in AD. Meanwhile, the levels of TGF-β1 produced by Tregs were significantly lower in AD, and anti-TGF-β1 abolished such suppression. Conclusion: The attenuated inhibitory ability of Tregs on hyper-activated autologousCD8+CLA+T cells, mediated by TGF-β1, plays an important role in the pathogenesis of AD.
