LB1475 The immune-phenotype of small plaque psoriasis

Small plaque psoriasis (SPP) presents as a unique morphology that resemble guttate psoriasis but lesions are larger, are chronic, and are not associated with streptococcal infection. We have observed SPP develop in four different population groups; patients under TNFα-inhibitor (TNFi) therapy, immune checkpoint inhibitor (ICI) therapy, and patients with concurrent SLE or ANA positivity and psoriasis. The pathogenesis of TNFi induced lesions are dominated by the type-1 interferon (IFN) pathway; increased expression of LL37 and IL36 by keratinocytes, activated plasmacytoid dendritic cells and release of type-1 IFN. These lesions express fewer epidermal CD8 T cells. We hypothesize that SPP develops as a result of increased expression of cytokines and antimicrobial peptides involved in the type-1 IFN pathway. Skin biopsies were obtained from patients with TNFi-induced psoriasis, SLE and psoriasis, positive ANA and psoriasis, ICI-induced psoriasis (n=12) and chronic plaque psoriasis as control (n=3). Immunohistochemistry was performed using antibodies against MXA, LL37, IL36 and CD8 T cells. Immunohistochemical evaluation revealed an increased expression of MXA (p<0.05), LL37 (p<0.05), IL36(p<0.05) in the keratinocytes of all clinical scenarios of SPP. There was decreased CD8 T cell migration to the epidermis in SPP. This is the first study to describe the immune-phenotype of SPP and to extend the phenotype observed in TNFi-induced psoriasis to varying clinical scenarios. There was an increased expression of cytokines in the type-1 IFN pathway as well as fewer epidermal CD8 T cell migration in SPP than in chronic plaque psoriasis. This immune-phenotypic analysis may suggest tailored therapy for this form of psoriasis.