Psoriasis has always been a common disease. Historically, its causes were obscure and surrounded by stigma; it wasn’t until recently that scientists categorized it as an autoimmune condition.
Psoriasis has always been a common disease. Historically, its causes were obscure and surrounded by stigma; it wasn’t until recently that scientists categorized it as an autoimmune condition. Indeed, modern scientific research shows that the body’s own T-cells, macrophages and dendritic cells are responsible for attacking healthy skin tissue, triggering inflammation and proliferation of skin cells, and resulting in the characteristic red, painful plaque-like lesions experienced by psoriasis patients.
But although these immune-mediating cells have been identified as the primary culprits for the breakdown of healthy skin, their roles do not fully clarify the underlying cause. What makes these cells behave so abnormally?
Based on their existing knowledge of the cellular and genetic pathways linked with the disease, Professor Kazumitsu Sugiura and Dr. Soichiro Watanabe from Fujita Health University, Japan, along with their colleagues, attempted to find out. Their study helped them clarify the role of another potential culprit in the formation of psoriasis lesions: neutrophils. Their findings are published in Scientific Reports.
Read more at: Fujita Health University
Microscopic observations of the back skins of two mice--one with the IL-36 deficiency and another wild type--after topical application of psoriasis-inducing imiquimod show that the former developed psoriasis like lesions after 3 days of application. They also showed greater neutrophil infiltration (Photo Credit: Kazumitsu Sugiura from Fujita Health University)
