What is the connection between autoimmunity and vitiligo? Over the years, many studies have been administered that suggest different causes of vitiligo. The most widely accepted hypothesis for the progressive loss of melanocytes (a mature melanin-forming cell) is the autoimmune theory. The theory proposes that, in vitiligo, the immune system reacts against the body’s own cells and tissues. This subsequently results in the destruction of melanocytes and manifests in white skin lesions.
Nonsegmental vitiligo, a more common type of vitiligo, accounts for between 90 and 95% of cases. This subtype of vitiligo is commonly associated with autoimmunity, unlike segmental vitiligo.
While autoimmunity is thought to be the initial pathogenic event in melanocyte destruction, studies that establish a link between autoimmunity and vitiligo so far have been administered with limited sample sizes and cross-sectional design. Therefore, more studies need to be conducted to establish that it is autoimmunity that causes vitiligo in the first place, not oxidative stress, toxins released by nerve ending, nutrition deficiency and genetics (that are considered possible vitiligo triggers by various researchers).
What existing studies suggest about autoimmunity in vitiligo
The epidemiological and clinical evidence, the chronic disorder’s frequent association with other organ-specific autoimmune disorders and a positive response to immunosuppressive treatments in people vitiligo work in favor of the autoimmune hypothesis of vitiligo.
Autoimmunity theory is sustained by several epidemiological, clinical, and laboratory studies. Elevated organ and non-organ-specific autoantibodies levels have been reported in the serum of research study participants with vitiligo. The frequency of such autoantibodies (an autoantibody is an antibody that is produced by the immune system to direct against one or more of the individual’s own proteins) varies according to different studies conducted so far.
Such autoantibodies have also been found in the basal layer of lesional vitiligo epidermis. However, autoantibodies’ role in people with vitiligo is still quite unknown, especially when they don’t display clinical signs of autoimmune-associated diseases.
Treatment of autoimmunity in vitiligo
Oral administration: Some drugs can be prescribed to increase the immune system’s antioxidant capacity of neutralizing and freeing radicals.
Topical Solution: Autoimmunity in vitiligo can be attempted to be cured with topical calcineurin inhibitors (immune-modulating medication) that work to prevent the body’s immune system from attacking pigment-producing melanocytes. Immunosuppressant creams can also be applied to suppress the immune response in the areas of skin where they are applied.
Laser Treatment: All kinds of laser treatments for vitiligo attempt to modulate the immune response, inducing melanocyte migration and proliferation (from the niche located in hair follicles) at the same time.
Narrowband UVB phototherapy: Narrowband UVB attempts to correct nonsegmental vitiligo by suppressing the immune system in the region to which it is applied. The procedure stabilizes the abnormal immune response by causing the death of the cells that are involved in the immune response. Narrowband UVB phototherapy also triggers the release of chemicals (which suppress the immune system and impair its aggression) and stimulates viable melanocytes within the depigmented area, which may have survived the attack of the immune system.
