Abstract
Recent studies have shown that vitiligo is a T-cell mediated autoimmune disease. Skin-homing cytotoxic T lymphocytes expressing cutaneous lymphocyte-associated antigen (CLA) have been suggested to be responsible for the destruction of melanocytes in vitiligo. An aberration in the suppressive function of regulatory T cells (Tregs) has been reported in vitiligo patients. However, whether the weakened suppressive ability of the Tregs contributes to hyper-activated skin homing CD8(+)CLA(+) T cells remains to be determined. To investigate the inhibition of circulating Tregs on the proliferation of autologous CD8(+)CLA(+) T cells in non-segmental vitiligo patients. CD8(+)CLA(+) T cells and Tregs were obtained from the peripheral blood of 13 non-segmental vitiligo patients and 7 controls. The proliferative responses of CD8(+)CLA(+) T cells were assessed in the absence or presence of autologous Tregs, and the levels of Transforming Growth Factor β1(TGF-β1) and IL-10 in culture supernatants were detected by enzyme-linked immunosorbent assay. The proliferative responses of circulating CD8(+)CLA(+) T cells in the presence of Tregs were significantly higher in the active vitiligo than in the stable vitiligo and control groups. Tregs from active vitiligo patients exhibited a lower inhibitory effect on proliferation of CD8(+)CLA(+) T cells. The levels of TGF-β1 produced by Tregs were significantly lower in active vitiligo than other groups and anti-TGF-β1 antibodies could abrogate the suppressive function of Tregs. The functional activity of Tregs is compromised in active vitiligo patients. TGF-β1 plays an important role in the autoimmune mechanism of the disease.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.