Psoriasis is an auto-inflammatory disease that affects skin and other organs and leads to the

impaired quality of life. Approximately 2 to 3% of the worldwide population suffers from this

debilitating condition, the causes of which are currently poorly understood. Keratinocytes are the

predominant cell type in the epidermis, the outermost layer of the skin. When activated, they can

stimulate cutaneous inflammation and abnormal keratinocyte behavior plays a role in the

pathogenesis of psoriasis. A gene called CARD14 has been identified as a psoriasis susceptibility

gene. However, little is known about the biochemical function and physiological role of the CARD14

protein.

We have recently shown that the paracaspase MALT1 interacts with CARD14 in keratinocytes and is

indispensable for signaling mediated by CARD14 and psoriasis-associated CARD14 mutants. The aim

of this project is to further characterize the role of CARD14 and the protease MALT1 in the

pathogenesis of psoriasis using mouse genetic engineering and mouse models of skin inflammation.