Alopecia Areata: A Review of Disease Pathogenesis

F. Rajabi; L.A. Drake; M.M. Senna; N. Rezaei

Disclosures

The British Journal of Dermatology. 2018;179(5):1033-1048. 

In This Article

Conclusions

The well-studied events of IP collapse, MHC presentation and the indispensable functions of IFN–γ are agreed upon among the majority of studies on the pathogenesis of AA, but as prelesional HFs also show features of IP breakdown[17,25,107] it seems that secondary immunological events are required to cause AA.[17] These events may involve cytotoxic T lymphocytes, Th17 cells, IL–15 or many other cell lines that were discussed earlier.

Although genetic studies for AA are considered to be far advanced, including genome-wide association studies and multiple-association studies, the existence of a humanized mouse model that develops AA deprived of any specific genetic background somehow questions the essentiality of a genetic base. Furthermore, the roles of MIF and AIRE in the pathogenesis of AA are still unclear.

It may be reasoned that AA is an independent medical entity with a large spectrum of manifestations, in addition to a common symptom associated with a diverse set of diseases.

Comments

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