Tu108 - An Inducible Mouse Model of Primary Cicatrcial Alopecia Exhibits Loss of CD200R

Khashayar Afshari – Post Doctoral Associate, Dermatology, University of Massachusetts Chan Medical School; Nazgol Sadat Haddadi – Post Doctoral Associate, Dermatology, University of Massachusetts Chan Medical School; Danny Kwong – Dermatology – University of Massachusetts Chan Medical School; Renee Joyce – Medical Student, University of Massachusetts Chan Medical School; Christine Li – Medical Student, University of Massachusetts Chan Medical School; Saeed Shakiba – Visiting Scholar, Dermatology, University of Massachusetts Chan Medical School; Jillian Richmond, Ph.D. – Assistant Professor, Dermatology, University of Massachusetts Chan Medical School

Abstract Text: Primary Cicatricial Alopecias (PCAs) are a group of autoinflammatory disorders characterized by scarring of the hair follicle. As a result, irreversible hair loss occurs. CD8+ T cells attack epithelial hair follicle stem cells (eHFSCs), and fibrosis ensues. We developed an inducible mouse model of alopecia that exhibits skin fibrosis using adoptive transfers of OT1 T cells into an autoimmune prone host mouse that expresses ovalbumin under the control of a keratin 5 promoter. We performed skin biopsies for histology, NanoString inflammation and immunology target gene expression and flow cytometry quantification of immune filtrates from mouse skin and compared these to human datasets. Comparison of gene expression in PCA mouse model to published human datasets revealed overlap with LPP, CCCA and DLE. Flow cytometry analysis of affected mouse skin exhibited significantly reduced CD200R expression. Previous studies suggest that the CD200-CD200R signaling pathway is immunoregulatory and protects the hair follicle from immune attack. We plan to continue examining hair follicle immune privilege breakdown as it pertains to autoinflammatory T cells, with the goal of identifying novel treatment targets for scarring alopecia.