Abstract
Psoriasis arises from poorly defined pathological crosstalk between keratinocytes and the immune system. BCL10 and MALT1 are ubiquitously expressed inflammatory signalling proteins that can interact with the psoriasis susceptibility factor CARD14, but their functions in psoriasis are insufficiently understood. To explore the roles of BCL10 and MALT1 in inflammatory skin diseases, we engineered a series of conditional mouse mutants to specifically activate, inactivate or attenuate BCL10/MALT1 signalling in keratinocytes in vivo.
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