LAUSR

EJD, vol. 28, n◦ 3, May-June 2018 to be heterogeneous and complex. The precise characterisation of autoantibodies may shed light on the pathogenesis of AHA [7]. Severe forms of psoriasis are associated with a decreased expression of negative immune regulatory genes, such as CTLA4 [8], which may favour the expression of autoimmune diseases, such as AHA [9]. GPP has been recognised as an autoinflammatory keratinization disease due to IL-36 receptor antagonist deficiency or CARD14 mutations/variants [10], and mechanisms of autoimmunity involving Th-17 cells have also been considered. Our patient represents an interesting association between an autoinflammatory keratinization disease and autoimmune disease.