Undergraduate Researcher California State Univ., San Marcos Vista, California, United States
Disclosure(s):
Dregyn Bennett: No financial relationships to disclose
Introduction/Rationale: Alopecia areata is a complex polygenic autoimmune disorder that affects approximately 160 million individuals worldwide, manifesting primarily as non-scarring, patchy hair loss. Current treatments utilizing JAK inhibitors necessitate prolonged use and are often accompanied by adverse side effects, such as increased headaches and a heightened risk of respiratory infections. Expanding therapeutic treatment options relies on a better understanding of the autoinflammatory mechanisms initiating and perpetuating alopecia areata. The C3H/HeJ inbred mouse strain is a well-established model for studying the pathogenesis of alopecia areata and validating experimental treatments. However, detailed knowledge of how the cellular immunophenotype in the skin changes during the stages of alopecia areata progression in C3H/HeJ mice is incomplete.
Methods: We performed immunofluorescence microscopy and flow cytometry to assess the prevalence of macrophages, dendritic cells, B cells, CD4 T helper cells, CD8 T cells and T cells around the hair follicle and surrounding dermis tissue at various stages of disease progression. Cell populations were quantified globally in the skin and per hair follicle.
Results: Findings indicate distinct immunophenotypic phases of alopecia areata. We defined these stages as: control with no signs of disease, prelesional disease, active disease, established disease, and regrowth. We have carefully immunoprofiled the skin and hair follicles in each of these stages to create an immune blueprint for mapping alopecia areata in natural disease of C3H/HeJ mice.
Conclusion: Chronologically ordering hair follicle attack pathogenesis may reveal therapeutic targeting of inflammation pathways causing alopecia areata in humans.
