Alopecia Areata: A Review of Disease Pathogenesis

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


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

In This Article

Evidence of Immune Privilege Collapse in Alopecia Areata

Many studies have succeeded in providing proof of the different aspects of IP breakdown in AA after it was first suggested by Paus et al. in 1993.[66] The actual presence of lymphocytes, dendritic cells and NK cells in the peribulbar area of the anagen HF, which is normally sparse of immune cells, is solid proof of IP collapse in AA.[8,67] Studies have demonstrated greater MHC-I and MHC-II expression in AA lesions than in normal HFs.[68–70]

It has also been shown that levels of IP guardians such as IDO, red/IK, TGF–β and α–MSH are lower in lesional or perilesional AA sites.[29,71] Upregulation of MICA,[49] chemokines (CXCLs), intercellular adhesion molecules (ICAM2 and ICAM3) and IFN–γ was also demonstrated in AA lesions.[71–73] IFN–γ is a powerful inducer of MHC, MICA, ICAM and NKG2D,[74,75] and an indispensable factor in AA pathogenesis that could trigger IP collapse and induce AA.[76–78]