Abstract
Abstract Psoriasis is a Th17-induced dermatitis, characterized by epidermal thickening. Psoriasis increases the risk of developing arthritis and cardiovascular-related morbidities, hence the need to stop its progression early. Why the disease is patchy, and what activates the keratinocytes in the psoriatic plaques driving a Th17-type inflammation, remain unknown. Chronic exposure to imiquimod (IMQ) drives psoriasis in mice reminiscent of human disease. We have preliminary data implicating the TNFSF (tumor necrosis factor superfamily) member TL1A (tumor necrosis factor-like cytokine 1A) in psoriasis. Our loss of function studies show that the genetic deletion of TL1A receptor, protects from IMQ-induced psoriasis. Further, TL1A is known to be enriched in the psoriatic lesions and serum of psoriatic patients. These findings suggest that TL1A may play a central role in the development and maintenance of psoriasis. Therefore, targeting TL1A could be beneficial to treat Psoriasis.
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