Participation of T cell immunoglobulin and mucin domain-3 (TIM-3) and its ligand (galectin-9) in the pathogenesis of act
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Participation of T cell immunoglobulin and mucin domain-3 (TIM-3) and its ligand (galectin-9) in the pathogenesis of active generalized vitiligo Manoj Kumar Tembhre • Anita Singh Parihar • Alpana Sharma • Somesh Gupta • Parthaprasad Chattopadhyay • Vinod Kumar Sharma
Ó Springer Science+Business Media New York 2015
Abstract Vitiligo is a depigmentary disease where melanocytes of the basal layer of epidermis are selectively destroyed by immune-cell-mediated cytotoxicity. The T cell immunoglobulin- and mucin-domain-containing molecules (TIMs) are involved in immune regulation, and their participation is not known in vitiligo. The present study revealed significant increase in the percentage of CD3?CD4? TIM3? T cells (P \ 0.05) in peripheral blood and was positively correlated with percentage body surface area involvement in aGV group. Further, increased expression of TIM-3 and its ligand galectin-9 (Gal-9) mRNA was found in peripheral blood and lesional/perilesional skin of active generalized vitiligo (aGV) compared with controls. Characteristic migration pattern of TIM-3-positive immune cells in lesional (near/in the epidermis) and perilesional (towards epidermis) skin section suggested that TIM-3? immune cells may be involved in melanocyte destruction. Further, investigation is required to understand the role of TIM-3/ Gal-9 signalling pathways in aGV and it can be targeted in the management of vitiligo. Keywords vitiligo
TIM-3/galectin-9 IFN-c IL-4 Generalized
Electronic supplementary material The online version of this article (doi:10.1007/s12026-015-8632-6) contains supplementary material, which is available to authorized users. M. K. Tembhre A. S. Parihar A. Sharma S. Gupta P. Chattopadhyay V. K. Sharma (&) All India Institute of Medical Sciences, New Delhi, India e-mail: [email protected]
Introduction Vitiligo is an autoimmune depigmentary disease where melanocytes of the basal layer of epidermis are the target and selectively destroyed leading to the patchy loss of pigmentation from the skin. Deregulated CD4? T cell function and autoreactive melanocyte-specific cytotoxic T cells have been reported in the pathogenesis of vitiligo supporting the autoimmune hypothesis [1–7]. Moreover, alteration in the specialized subpopulation of CD4? T cells, T helper 1 (Th1), Th2, Th17 and regulatory T cells (Tregs), has been implicated in the pathogenesis of vitiligo [1–10]. Recent evidences have shown that there is deregulation in the immune regulatory components such as deficiency in frequency, function and homing of regulatory T cells along with altered Th cell cytokines [11–15]. The T cell immunoglobulin- and mucin-domain-containing molecules (TIMs) are newly described group of type I membrane glycoprotein molecules with a conserved structure having an IgV domain, highly glycosylated mucin domain and cytoplasmic domain [16, 17]. TIMs are implicated in wide variety of immunological functions, including T cell activation, induction of T cell apoptosis and T cell tolerance, and the clearance of apopto
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