CD80CD86 deficiency disrupts regulatory CD4+FoxP3+T cell homoeostasis and induces autoimmune-like alopecia

Abstract Alopecia areata ( AA ) is an autoimmune disease that results in spot baldness in humans. Adequate animal models for AA are currently lacking. The objective of this study was to elucidate the mechanism of autoimmune‐like alopecia ( ALA ) in C57 BL /6. CD 80 CD 86‐deficient (B6. CD 80 CD 86 −/− ) mice. Incidence and severity of alopecia were analysed in 58 B6. CD 80 CD 86 −/− mice using histological examination, flow cytometry, multiplex enzyme‐linked immunosorbent assay, quantitative RT ‐ PCR and CD 25 inhibition test. Both male and female B6. CD 80 CD 86 −/− mice showed almost 100% incidence of hair loss at 40 weeks of age. Moreover, CD 4+FoxP3+Treg (Treg) cell population in B6. CD 80 CD 86 −/− mice was significantly lower than in B6 mice, which presumably underlined autoimmune reaction. Histologically, B6. CD 80 CD 86 −/− mice showed CD 4+ and CD 8+ T‐cell infiltration around terminal follicle region and exhibited hair follicle destruction in the anagen or catagen stage. Negative correlation between the number of CD 4+FoxP3+ Tregs and ALA was confirmed by the CD 25 depletion test in B6 mice, as follicle destruction was similar to that observed in B6. CD 80 CD 86 −/− animals. CD 80 CD 86 deficiency disrupted CD 4+FoxP3+ Treg homoeostasis and prompted the development of ALA . We demonstrated that B6. CD 80 CD 86 −/− mice might have several advantages as an ALA model, because they exhibited high incidence of disease phenotype and epipathogenesis similar to that observed in human AA .