140 Comparative scRNA-Seq profiling of four autoimmune skin diseases points to CXCL13 as a potential player in skin autoimmunity
نویسندگان
چکیده
Autoimmune diseases are caused by loss of self-tolerance resulting in both humoral and cell-driven targeting healthy tissue immune cells. Different cytokines thought to drive different autoimmune skin (e.g. IL17 psoriasis, Type-I interferon cutaneous lupus erythematosus (CLE), Type-II vitiligo), yet similar cytokine signatures present across diseases. For a direct systematic comparison disease signatures, we used single-cell RNA-Seq profile lesional nonlesional skins from patients with dermatomyositis (DM), CLE, or vitiligo. We found that CXCL13 was among the most upregulated, lesion-specific genes T cells, drastically higher DM, confirmed OLINK. Despite up all cells subtypes, subsets had strongest expression (IL17+ CD8 RDH10+GZMK- CD200+ CD4 other diseases). is not pan-inflammatory cytokine. Steven-Johnson syndrome contact dermatitis have undetectable levels. known be secreted helper recruit activate CXCR5+ B at secondary tertiary lymphoid organs. However, vitiligo psoriasis cell-mediated, no skin. Interestingly, identified CXCR5+CXCR3- set peripheral blood as candidate for CXCL13-specific recruitment. In section staining, CXCL13+ co-localize pathological angiogenesis, CXCL13+CD4 surrounding vessels DM CLE while CXCL13+IL17+CD8 dermis protruding into epidermis, where angiogenesis happens. As induction, in-vitro type-I but type-II IFN stimulation upregulated activated Taken together, our study suggests has disease-specific patterns may functions than supporting B-cells.
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ژورنال
عنوان ژورنال: Journal of Investigative Dermatology
سال: 2023
ISSN: ['1523-1747', '0022-202X']
DOI: https://doi.org/10.1016/j.jid.2023.03.141