Vitiligo is a skin condition that causes the skin to lose its color or pigment. This causes the skin to appear lighter than the natural skin tone or turn white. Areas of the skin that lose their pigment are called macules if they’re less than 1 centimeter wide, or patches if they’re larger than 1 centimeter. The amount of affected skin varies for each person diagnosed. Some experience a few depigmented areas, while others have widespread loss of skin color.
Vitiligo is a complex condition that occurs when the body’s immune system destroys melanocytes. Melanocytes are skin cells that produce melanin, the chemical that gives skin its color, or pigmentation. It usually starts with a few small white macules or patches that gradually spread over the body. It typically begins on the hands, forearms, feet and face, but can develop on any part of the body. Sometimes, larger patches continue to widen and spread but can stay in one place for years.
Oxidative Stress
The pathogenesis of the condition results from the interaction of genetic components, metabolic factors linked to cellular oxidative stress, melanocyte adhesion to the epithelium, and immunity, which culminate in aggression against melanocytes. In individuals with vitiligo, melanocytes are more sensitive to oxidative damage, leading to increased expression of proinflammatory proteins. It is hypothesized that oxidative stress inflicts cell damage by inducing apoptosis in melanocytes.
Innate and Adaptive Immunity
Dendritic cells, macrophages, and NK cells are found in the lesional skin of patients with vitiligo characterizing an activation of the innate immune response. The oxidative stress that occurs in the melanocyte, as mentioned above, can cause damage to the melanocytes and is possibly the autoimmunity trigger in vitiligo.
The activation of innate immunity triggered by damage to melanocytes affected by oxidative stress promotes cytokine secretion and antigen presentation, resulting in the adaptive immune system activation, in which autoreactive T-cells amplify damage to melanocytes in vitiligo-affected skin. Cytotoxic CD8+ T-cells are necessary and sufficient for the destruction of melanocytes, acting as an effector arm of autoimmunity. The lesions are caused by effector CD8+ T-lymphocytes in the initial or active phase of the disease and by recirculating and resident memory CD8 + T (TEM) lymphocytes in the stable phase.
CD4+ T-regulatory cells (Tregs) act to maintain tolerance to their own tissues by suppressing the activity of T-effector cells. In vitiligo, there is a Treg dysfunction, although it is not known exactly whether due to the inability to migrate to the skin, decreased numbers, or activity suppression.
