TNFR2+ Epidermal γδ T Cell Function in Psoriasis

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Presentation Time: 11:30 AM - 12:45 PM
Poster Board Number: B915
Abstract ID: 4328

Presenting Author:
Patricia A Tulloch , Undergraduate Researcher at California State Univ., San Marcos

Abstract:

Psoriasis impacts 2-3% of people worldwide resulting in thick patches of skin that itch or burn. The inflammatory response associated with psoriasis involves the TNF- α/IL-17/IL-23 axis and biologics targeting these cytokines show success in improving disease. Dermal αß and γδ T cells have been implicated in producing IL-17, however, less is known about roles played by resident epidermal T cells. While a small subset of resident epidermal γδ T cells produce IL-17 during wound repair and UV treatment, their role in psoriasis is less understood. Here we examine the role of TNF- α in regulating inflammatory roles played by subsets of epidermal γδ T cells during psoriasis. Upon activation, a subset of epidermal γδ T cells upregulates TNFR2, but does not upregulate TNFR1. While TNFR1 and TNFR2 are not required for epidermal γδ T cell seeding or homeostasis in the skin, addition of TNF- α induces a Th17 focused response by epidermal γδ T cells. This finding is confirmed upon examination of publicly available ssRNAseq data showing that TNFR2-expressing epidermal γδ T cells differentially express IL-17A during psoriasis. Together these data highlight a subset of epidermal γδ T cells that are receptive to TNF- α through TNFR2 inducing IL-17 production in psoriasis. Thus, epidermal resident T cells also participate in exacerbation of disease and represent targets for treatment.