Alopecia areata
● Symptoms and Causes
In AA, stimulatory factors may activate CD8 + NKG2D + T cells and produce IFN-γ via JAK1 and JAK3 pathways. IFN-γ can enhance the production of IL-15 in follicular epithelial cells through JAK1 and JAK2. IL-15 then binds to the CD8 + NKG2D + T cells to produce more IFN-γ, which amplify the positive feedback loop. IFN-γ promotes hair follicle immune privilege collapse, which leads to exposure of autoantigens to CD8+NKG2D+ T cells and facilitates the autoimmune attack on hair follicles. Meanwhile, other inflammatory cells, such as DCs, CD4 + T cells, NK T cells, mast cells, and eosinophils, accumulate around hair bulbs.
Zhou, C., Li, X., Wang, C. et al. Alopecia Areata: an Update on Etiopathogenesis, Diagnosis, and Management. Clinic Rev Allerg Immunol 61, 403–423 (2021). https://doi.org/10.1007/s12016-021-08883-0
Alopecia areata
● Symptoms and Causes
In AA, stimulatory factors may activate CD8 + NKG2D + T cells and produce IFN-γ via JAK1 and JAK3 pathways. IFN-γ can enhance the production of IL-15 in follicular epithelial cells through JAK1 and JAK2. IL-15 then binds to the CD8 + NKG2D + T cells to produce more IFN-γ, which amplify the positive feedback loop. IFN-γ promotes hair follicle immune privilege collapse, which leads to exposure of autoantigens to CD8+NKG2D+ T cells and facilitates the autoimmune attack on hair follicles. Meanwhile, other inflammatory cells, such as DCs, CD4 + T cells, NK T cells, mast cells, and eosinophils, accumulate around hair bulbs.
Zhou, C., Li, X., Wang, C. et al. Alopecia Areata: an Update on Etiopathogenesis, Diagnosis, and Management. Clinic Rev Allerg Immunol 61, 403–423 (2021). https://doi.org/10.1007/s12016-021-08883-0