Alopecia areata: A multifactorial autoimmune condition

Abstract

Highlights  Alopecia areata is a polygenic and multifactorial autoimmune disease characterised by non-scarring hair loss.  Autoreactive CD8 + , CD4 + , natural killer cells and plasmacytoid dendritic cells infiltrate around the hair follicles during the growth (anagen) phase.  Increased cytokine activity, particularly IFN-γ, results in disruption of the hair follicle immune privilege and premature termination of the anagen phase, followed by hair follicle atrophy and dystrophy in persistent disease.

The Potential Application of Ecklonia cava Extract in Scalp Protection

“…The scalp is exposed to various irritants such as detergents, microorganisms, dry climate and urban dust [16], and irritation often results from residual detergents and dysregulation of microbiota [17]. Scalp dandruff is primarily attributed to Malassezia yeasts, which are known to provoke upregulation of inflammatory mediators such as IL-8, are chemotactic to neutrophils and irritating fatty acid [18].…”

No Increased Risk of Alopecia in Ankylosing Spondylitis Patients: A Population-based Cohort Study in Taiwan

“…Elevation of certain cytokine levels in circulation was observed in AS patients, such as IL-12, IL-17, and IL-23 [26][27][28][29][30][31]. Also, elevation in IL-12 and IL-23 was noted in patients with alopecia areata [4,5,32]. Though the increase in circulatory cytokine level has something to do with one's systemic inflammatory response and overall immunity, this may not imply a direct association between AS and alopecia.…”

“…The androgen level in AS patients remains controversial [2]. Alopecia may be genetic, psychogenic, androgenetic, autoimmune [3][4][5], iatrogenic, idiopathic, etc. It can be limited over the forehead, be patchy, or extends to whole body hair loss.…”

Alopecia Areata after Omalizumab Treatment for Chronic Spontaneous Urticaria

“…Although hair loss is listed among the side-effects in the SmPC of omalizumab, all previous reports related to diffuse and transient types of hair loss and not to AA (5,6). AA represents a multifactorial autoimmune organ-specific disease and its pathogenesis involves T-cell autoantigens, type 1 T helper (Th1)/interferon-γ, Th2, PDE4, interleukin (IL)-23 and IL-9 pathways (7). It can be speculated that the downregulation of Th2 pathways might amplify the Th1 pathway and promote the development of AA with omalizumab use (8).…”