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Alopecia Areata: an Update on Etiopathogenesis, Diagnosis, and Management

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Abstract

Alopecia areata (AA) is a common chronic tissue-specific autoimmune disease, resulting in hair loss, that affects up to 2% of the general population. The exact pathobiology of AA has still remained elusive, while the common theory is the collapse of the immune privilege of the hair follicle caused by immunological mechanism. Multiple genetic and environment factors contribute to the pathogenesis of AA. There are several clinical treatments for AA, varying from one or multiple well-defined patches to more diffuse or total hair loss of the scalp (alopecia totalis) or hair loss of the entire body (alopecia universalis). The available treatments for AA, such as corticosteroids and other immunomodulators, minoxidil, and contact immunotherapy, are of limited efficacy with a high risk of adverse effects and high recurrence rates, especially for patients with severe AA. Recent insights into the pathogenesis of AA have led to the development of new treatment strategies, such as Janus kinase (JAK) inhibitors, biologics, and several small molecular agents. In addition, modern therapies for AA, including antihistamines, platelet-rich plasma (PRP) injection, and other novel therapies have been well explored. In this review, we discussed the recent advances in the pathogenesis, diagnosis, and treatment of AA.

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Abbreviations

AA:

Alopecia areata

AAI:

Alopecia areata incognita

AA-IGA™:

AA investigator global assessment

AD:

Atopic dermatitis

ADTA:

Acute diffuse and total alopecia

AT:

Alopecia totalis

AU:

Alopecia universalis

α-MSH:

α-Melanocyte-stimulating hormone

cAMP:

Cyclic adenosine monophosphate

CI:

Contact immunotherapy

CNV:

Copy number variant

CTLA4:

Cytotoxic T lymphocyte–associated antigen 4

CXCL:

Chemokine ligand

DPCP:

Diphenylcyclopropenone

ERK:

Extracellular signal–regulated kinase

GWAS:

Genome-wide association studies

HF:

Hair follicle

HLA:

Human leukocyte antigen

IC:

Intralesional corticosteroids

IFN:

Interferon

IL:

Interleukin

IP:

Immune privileged

JAK:

Janus kinase

JAKi:

JAK inhibitors

MHC:

Major histocompatibility complex

MICA:

MHC class I–related chain A

NK:

Natural killer

PBMC:

Peripheral blood mononuclear cell

PCT:

Pulse corticosteroid therapy

PDE:

Phosphodiesterase

PRP:

Platelet-rich plasma

RCT:

Randomized controlled trial

ROS:

Reactive oxygen species

SADBE:

Squaric acid dibutyl ester

SALT:

Severity of alopecia tool

SOD:

Superoxide dismutase

STATs:

Signal transducers and activators of transcription

TA:

Triamcinolone acetonide

TC:

Topical corticosteroids

TGF:

Transforming growth factor

TNF:

Tumor necrosis factor

Tregs:

T-regulatory cells

TYK2:

Tyrosine kinase 2

ULBP:

UL16-binding protein

VIP:

Vasoactive intestinal peptide

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Funding

This study was supported by the National Natural Science Foundation of China (No. 82073459 and No. 81773311).

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  1. Cheng Zhou and Xiangqian Li contribute equally to this work.

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  1. Department of Dermatology, Peking University People’s Hospital, No. 11 Xizhimen South Street, Xicheng District, Beijing, China

    Cheng Zhou, Xiangqian Li, Chen Wang & Jianzhong Zhang

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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

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