The Role of the NKG2D in Vitiligo

Vitiligo is an acquired multifactorial disease that affects melanocytes and results in skin depigmentation. In this review, we examine the role of cells stress and self-reactive T cells responses. Given the canonical and non-canonical functions of NKG2D, such as authenticating stressed target and enhance TCR signaling, we examine how melanocyte stress leads to the expression of ligands that are recognized by the activating receptor NKG2D, and how its signaling results in the turning of T cells against self (melanocyte suicide by proxy). We also discuss how this initiation phase is followed by T cell perpetuation, as NKG2D signaling results in self-sustained long-lasting T cells, with improved cytolytic properties.

Automated summary

Vitiligo is an acquired multifactorial disease that affects melanocytes, leading to skin depigmentation. This review focuses on the role of cell stress and self-reactive T cells responses in the development of vitiligo, specifically looking at the NKG2D signaling pathway. The study discusses how melanocyte stress induces the expression of ligands recognized by NKG2D, leading to T cell activation against self.