CD80CD86 Deficiency Disrupts Regulatory CD4+FoxP3+ T Cell Homeostasis and Induces Autoimmune-Like Alopecia

April 2017 in “ Experimental dermatology ”

Ji‐Hyun Bae, Wu Jeong Hwang, Yongwoo Jang, Y. Lee, Da‐Eun Jang, J.H. Kim, Su Cheong Yeom

autoimmune-like alopecia CD80CD86 deficiency CD4+FoxP3+ regulatory T cells Tregs CD4+ T-cell infiltration CD8+ T-cell infiltration hair follicle destruction alopecia areata ALA regulatory T cells T-cell infiltration hair loss autoimmune alopecia

TLDR CD80CD86 deficiency causes hair loss by disrupting regulatory T cells.

The study investigated autoimmune-like alopecia (ALA) in CD80CD86-deficient (B6.CD80CD86−/−) mice, revealing that nearly 100% of these mice experienced hair loss by 40 weeks of age. The deficiency led to a significant reduction in CD4+FoxP3+ regulatory T cells (Tregs), which is believed to trigger autoimmune reactions. Histological analysis showed CD4+ and CD8+ T-cell infiltration and hair follicle destruction. The study confirmed a negative correlation between Treg numbers and ALA severity. The findings suggested that B6.CD80CD86−/− mice could serve as a valuable model for studying ALA due to their high disease incidence and similarities to human alopecia areata.

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Research cited in this study

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