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Frontiers in alopecia areata pathobiology research
Amos Gilhar1, Rimma Laufer-Britva2, Aviad Keren1
1Skin Research Laboratory, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
The Journal of Allergy and Clinical Immunology
|October 14, 2019
Summary
New research reveals that natural killer (NK) cells and unconventional T cells, not just CD8+ T cells, drive alopecia areata (AA) pathogenesis. Understanding immune privilege defects offers new therapeutic targets for AA.
Area of Science:
- Immunology
- Dermatology
- Pathobiology
Background:
- Alopecia areata (AA) is an autoimmune disorder primarily attributed to CD8+ T cell activity.
- Current understanding of AA pathogenesis is incomplete, necessitating exploration of novel contributing factors.
Purpose of the Study:
- To review emerging research on less-investigated aspects of alopecia areata (AA) pathobiology.
- To highlight potential new cellular players and immune mechanisms involved in AA.
- To identify novel therapeutic targets for AA.
Main Methods:
- Review of current scientific literature on AA pathobiology.
- Analysis of emerging evidence on immune cell subsets and their roles in AA.
- Exploration of the concept of immune privilege (IP) in hair follicles.
Main Results:
- Evidence suggests that natural killer (NK) cells and unconventional T cells (e.g., iNKT, γδ T, cNK, ILC1) may drive AA independently of CD8+ T cells.
- These cells produce significant amounts of IFN-γ, contributing to AA.
- Defects in regulatory lymphocyte subsets (e.g., Treg, γδ Treg, NKT10, mast cells) may impair hair follicle immune privilege (IP) in AA patients.
Conclusions:
- AA pathogenesis involves a broader range of immune cells than previously understood.
- Restoring hair follicle immune privilege (IP) presents a potential therapeutic strategy for AA.
- Findings may also inform treatments for other autoimmune disorders involving immune privilege collapse.
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