JLE

European Journal of Dermatology

MENU

Characterization of circulating CD8+T cells expressing skin homing and cytotoxic molecules in active non-segmental vitiligo Volume 23, issue 3, May-June 2013

Figures

See all figures

Authors
Department of Dermatology,, Department of Clinical Laboratory, 2 nd Affiliated Hospital, Dalian Medical University, 467 Zhongshan Road, 116027 Dalian, Liaoning Province, P. R. China;, Dermatology, Northern California Institute for Research and Education, San Francisco, CA 94121, USA, Department of Dermatology, Yidu Central Hospital, Weifang Medical University, 262500 Qingzhou Shandong Province, China, College of Integrative Medicine, Dalian Medical University, 116044 Dalian, Liaoning Province, China

Background: Vitiligo is caused by melanocyte depletion. Studies have suggested that skin-homing cytotoxic T lymphocytes that express cutaneous lymphocyte-associated antigen (CLA) are responsible for melanocyte depletion. The characteristics of these skin-homing cytotoxic T cells have not been well established yet. Objectives: To investigate the frequency of skin-homing CD8 +T cells (CD8 +CLA +T cells) and their expression of cytotoxic molecules, as well as migration-related molecules in CD8 +T cell in non-segmental vitiligo patients. Materials & Methods: The frequency of CD8 +CLA +T cells and their expression of cytotoxic molecules (perforin, granzyme-B and FasL) in peripheral blood of patients with non-segmental vitiligo were assessed using flow cytometry. Levels of chemokine receptors (CCR4, CCR10) on CD8 +T cells were evaluated. Results: Our results revealed a higher frequency and increased expression of perforin and granzyme-B in circulating CD8 +CLA +T cells from patients with active vitiligo. The expression levels of CCR4 increased in CD8 +T cells in active vitiligo patients. Conclusion: Patients with active non-segmental vitiligo have a higher frequency of CD8 +CLA +T cells and hyper-activated cytotoxic functions, which may be involved in the pathogenesis of non-segmental vitiligo.