The function of BST2 in γδ T Cells, CD8 T Cells, and macrophages in alopecia areata pathogenesis 4231

Abstract Description Alopecia areata is an autoimmune disease characterized by non-scarring hair loss, affecting 147 million individuals globally with a lifetime incidence of 2.1 percent. Cytotoxic CD8 T lymphocytes and helper CD4 T cells compromise hair follicle immune privilege in alopecia areata. Here we investigate the role of skin γδ T cells and macrophages in disease pathogenesis. Our findings reveal epidermal γδ T cells and keratinocytes are elevated in the skin of C3H/HeJ mice with alopecia. Publicly available single-cell RNA sequencing data delineated the top differentially expressed genes of epidermal γδ T cells, dermal Cd11b+ macrophages, and CD8 T cells. Bone marrow stromal antigen-2 (BST2) was identified as a significantly upregulated gene among all three cell types. To investigate BST2 function, we categorized cells into BST2+ and BST2- groups and performed differential expression analysis. Epidermal γδ T cells and CD8 T cells express antiviral and interferon response genes. Cd11b+ macrophages upregulate antiviral and interferon pathways, with BST2+ macrophages also upregulating complement-associated genes. Immunofluorescence microscopy confirmed increased BST2 expression by epidermal γδ T cells, CD8 T cells and macrophages in C3H/HeJ mice with alopecia areata. Future studies will elucidate the role BST2 plays in initiating pathogenesis of disease and further explore the interplay between epidermal γδ T cells, CD8 T cells and macrophages in alopecia areata. Funding Sources NIH R15DK127440 Topic Categories Basic Autoimmunity (BA)