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In this study, the researchers identified a variant in the CCHCR1 gene associated with an alopecia areata subtype characterized by impaired keratinization and autoimmune events.

This study identified that mouse MILL1 and MILL2 are glycoproteins distinct from human MICA/B, primarily due to their association with β2-microglobulin and TAP-independent surface expression.

This study found that diphencyprone showed a significant clinical response for treating alopecia areata, while tacrolimus was not effective.

This paper proposes that the induction of HF-specific neo-antigens by peripheral CD8+ T cells may maintain self-tolerance but could also lead to immunopathology in conditions like alopecia areata.

This study identified a specific genetic variant in the CCHCR1 gene that may contribute to alopecia areata through impaired keratinization, suggesting an alternative mechanism beyond autoimmune causes.