Vitiligo is an autoimmune disease in which the immune system mistakenly attacks melanocytes, the cells located at the dermo-epidermal junction responsible for the production of melanin, a pigment that protects the skin from UV rays. When the immune system is functioning properly, melanin is transferred to keratinocytes, which are involved in the inflammatory response. Two main mechanisms explain this loss in vitiligo: the destruction of melanocytes by CD8+ T lymphocytes and their apoptosis, as well as a defect in melanocyte adhesion, leading to their detachment from the basal lamina.
Vitiligo is not a contagious disease.
It does not result from a viral, bacterial, or fungal infection, nor from a transmissible pathogen like contagious diseases, and cannot be transmitted through physical contact, air, or blood. Dermatological and immunological studies confirm that vitiligo is strictly non-transmissible, as it is based on an internal malfunction of the immune system and not on an external agent.
However, genetic predispositions do exist for vitiligo and can cause confusion. Indeed, according to various sources, 20% of people affected by vitiligo have at least one first-degree relative with this disease, and these individuals are 7 to 10 times more likely to develop vitiligo. Over 50 susceptibility genes, including HLA, CTLA4, NLRP1, and TYR, have been associated with the disease. Individuals carrying variants of these genes have an increased risk of developing vitiligo, but they are not systematically affected. However, heredity alone is not sufficient as environmental factors can also play a role, including stress, the Koebner phenomenon, or even chemicals.