Understanding How Immune System Dysfunctions Trigger Vitiligo

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Vitiligo is caused by an autoimmune reaction against melanocytes leading to melanocyte loss. The cause of vitiligo is an interaction between genetic susceptibility and environmental factors as shared by Dr Rashmi Aderao, dermatology consultant at Ruby Hall Clinic Pune.

Currently, the exact aetiology of vitiligo remains obscure, but many factors have been implicated in the development of the disease including infections, stress, neural abnormalities, defective melanocyte adhesion, and genetic susceptibility. The biochemical hypothesis argues that melanocyte destruction is due to the accumulation of toxic metabolites from melanogenesis, the breakdown of free-radical defence, and an excess of hydrogen peroxide.

• External Factors: Trauma, sunburn, and exposure to certain chemicals can precipitate or worsen vitiligo by inducing oxidative stress and inflammatory responses.

• Infections: Viral and bacterial infections might trigger immune responses that cross-react with melanocytes.

Regulatory T Cells (Tregs): These cells normally suppress autoimmune responses, but their function may be impaired in vitiligo patients, allowing the immune system to attack melanocytes.

Melanocyte Defects: Intrinsic Defects: Melanocytes in vitiligo patients might have inherent defects making them more susceptible to immune attacks.

• Antigen Presentation: Abnormal presentation of melanocyte antigens could trigger an inappropriate immune response.

Both the adaptive immune system—through cytotoxic CD8+ T cells and melanocyte-specific antibodies—and the innate immune system are involved in the autoimmune process against melanocytes.

Skin melanocytes of vitiligo patients have an increased sensitivity to endogenous or external stress factors, such as trauma or ultraviolet radiation, which increase the production of reactive oxygen species (ROS) vitiligo melanocytes exhibit several structural defects that impair their ability to resist oxidative stress, including endoplasmic reticulum dilatation, mitochondrial dysfunction, and abnormal melanosome structure. However, the exact events leading to the development of vitiligo are still incompletely understood.

Vitiligo is linked to other autoimmune diseases, such as rheumatoid arthritis, thyroid diseases, and lupus, alopecia areata, IBD.

People with vitiligo may also have an increased risk of other autoimmune conditions, such as pernicious anemia, Addison's disease, and Sjogren's disease. Ideally, the management of vitiligo focuses on stopping the immune destruction of melanocytes, halting depigmentation, stimulating repigmentation, and preventing relapses