Vitiligo is a chronic disease of the epidermis characterized by the depigmentation of certain areas of the skin and hair. How can the occurrence of vitiligo be explained? Discover the biological mechanisms at work here.
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- What causes vitiligo?
What causes vitiligo?
Vitiligo: What are its causes?
Vitiligo is a condition affecting 0.5% to 2% of the global population. This multifactorial disorder is characterized by the loss of melanocytes , the cells capable of producing melanin, the pigment that protects the skin from UV rays. Several mechanisms may work together to contribute to the destruction of these melanocytes by self-reactive cytotoxic CD8+ T lymphocytes. Vitiligo depigmentation is primarily observed on the hands, face, and torso. It can appear at any age but is more common in younger individuals. It affects both men and women, regardless of skin type. Fortunately, vitiligo is not contagious, is painless, and does not cause any discomfort on the skin but is more vulnerable to sunlight. The affected area should always be protected from UV rays.
The primary causes of vitiligo have not yet been clearly determined. However, various genetic and non-genetic factors have been identified as triggers for its onset.
Genetic factors contributing to the onset of vitiligo.
Although vitiligo is not classified as a hereditary disease, familial predispositions are proposed as an explanation. Indeed, it has been noted that 20% of people affected by vitiligo have at least one first-degree relative with this disease, and there is a 7 to 10 times higher chance of being affected by vitiligo if you have a first-degree relative with this disease. According to numerous research studies, more than 50 susceptibility genes have been associated with vitiligo, and individuals carrying one or more variants of these genes are at a higher risk of developing it, although they are not systematically affected.
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A mechanism primarily autoimmune in nature is at the root of vitiligo.
Vitiligo is a so-called autoimmune disease, meaning it results from a malfunction of the immune system that attacks the normal constituents of the body. As mentioned earlier, when the disease appears, the epidermis responds by producing numerous danger signals recognized by the immune system. T lymphocytes, which are immune cells, are then activated and produce cytokines, inflammatory molecules that attack and degrade the melanocytes.
The mechanism works as follows: during the initiation phase, that is, on skin without lesions, vitiligo is triggered by genetic predispositions and certain environmental factors that activate danger signals and alert the immune system. The cells of the immune system detect these signals and release inflammatory messengers, the cytokines (IFN-α and IL-12). They then induce the production of chemokines CXCL9 and CXCL10, proteins that will recruit other immune cells from the blood. The activated immune cells release other inflammatory cytokines like IFN-γ and TNF-α, which attack the melanocytes, leading to depigmentation on the skin.
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Thus, although the exact causes of vitiligo are not fully understood, it is clear that genetic and immune factors play a major role in its development. However, certain environmental factors, such as oxidative stress, exposure to mites, or even skin trauma, could also exacerbate vitiligo and accelerate depigmentation. Understanding these triggers could allow for the adoption of strategies to prevent vitiligo.
Sources
SPRITZ R. A. & al. Genome-wide association studies of autoimmune vitiligo identify 23 new risk loci and highlight key pathways and regulatory variants. Nature genetics (2016).
EZZEDINE K. & BERGQVIST C. Vitiligo : A Review. Dermatology (2020).
BOUKHEDOUNI N. Mécanismes immunologiques impliqués dans la perte des mélanocytes au cours du vitiligo. Médecine humaine et pathologie. Université de Bordeaux (2018).
SPRITZ R. & al. The Genetic Basis of Vitiligo. Journal of Investigative Dermatology (2021).
Physiopathologie et mécanismes à l’origine du vitiligo. Vitiligo Bordeaux-Service de recherche clinique.
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