The Genetics of Psoriasis
Updated: Jun 14
By Katelin Wu
When discussing autoimmune diseases, most people tend to associate them with conditions like Multiple Sclerosis or Rheumatoid Arthritis. In essence, autoimmune diseases occur when our body's immune system, designed to target foreign pathogens, instead attacks our own healthy cells. For instance, individuals with Multiple Sclerosis face sensory issues as their immune systems target the myelin, a protective covering for nerve fibers. Similarly, those with Rheumatoid Arthritis suffer from joint pain due to the immune cells attacking healthy joint tissues. Surprisingly, one autoimmune disorder that often goes unnoticed is Psoriasis.
Affecting approximately 3% of the human population, psoriasis is a chronic autoimmune disease that has yet to be cured. Since it’s an autoimmune disease, the immune system mistakenly targets healthy skin cells as foreign invaders, triggering an accelerated production of skin cells. This overproduction leads to the formation of thick, red patches covered with silvery scales, known as psoriasis plaques. These plaques often cause itching and discomfort, and over time, they can result in dry and cracked skin. Psoriasis typically emerges during the ages of 15 to 35, affecting a significant portion of the population. Though, it’s worth noting that individuals with psoriasis need not be concerned about transmitting the condition to others as it is not contagious.
Multiple studies have shown that psoriasis tends to run in families, with a higher risk of developing the disease if one or both parents have it. Specific genetic variations have been identified as risk factors for psoriasis. The most well-known genetic marker associated with psoriasis is a variation in the HLA-C gene, which plays a role in regulating the immune system. This variation is known as HLA-Cw6 and is found more frequently in individuals with psoriasis. Additionally, researchers have discovered that psoriasis is strongly linked to a gene mutation, CARD14. Caspase Recruitment Domain Family Member 14 is a gene involved in regulating immune responses and inflammatory pathways. Mutations in the CARD14 gene can lead to an overactive immune response and abnormal inflammatory processes, contributing to the development of psoriasis. Research has shown that certain mutations in the CARD14 gene are more prevalent in individuals with psoriasis compared to those without the condition.
Furthermore, the development of psoriasis is a complex interplay between genetic predisposition and environmental triggers. While genetic predispositions can increase the risk of developing psoriasis, various specific environmental factors can activate the genes associated with psoriasis. For example, stress, infections, climate/humidity, medications, etc. are all common environmental triggers of psoriasis. Stress triggers physiological responses that disrupt immune regulation, leading to an overactive immune response and increased inflammation. This inflammatory response can worsen existing psoriasis symptoms or contribute to the development of new flare-ups. While stress doesn’t directly cause psoriasis, it plays a significant role in triggering or exacerbating the condition in individuals who are genetically predisposed.
In conclusion, genetics play a crucial role in the development of psoriasis. Numerous studies have highlighted the genetic component of psoriasis, with specific variations and mutations in genes like HLA-C and CARD14 associated with increased susceptibility to the condition. Further research into the genetic underpinnings of psoriasis will continue to shed light on the complex interactions between genes, immune system function, and environmental factors, ultimately improving our understanding and management of this chronic skin disorder.
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