Does Complement Have a Role in the Pathogenesis of Alopecia Areata?

Abstract

Alopecia areata (AA) is an autoimmune disorder in which immune attack of the anagen follicle causes hair loss in approximately 2% of the population. Although the pathogenesis of AA has not been fully determined, most likely it is mediated by a variety of factors including cellular/humoral immunity and genetic predisposition. Researchers have been interested in the possible role of the complement pathway in AA since the 1970s. Given recent evidence suggesting that complement plays a role in many immunologic and inflammatory dermatologic diseases including systemic lupus erythematosus, bullous diseases, angioedema, lipodystrophy, and skin infections, it is likely that complement also contributes to AA pathogenesis. Although early serum studies and immunohistochemical staining have been unimpressive, recent genetics studies may provide evidence that complement does indeed contribute to AA. By determining if complement plays a role in AA, options for novel targeted treatments will become available for those patients with refractory disease.

Identification of Distinct Immune Signatures and Chemokine Networks in Scalp Inflammatory Diseases

“…Besides, upregulation of intestinal immune network for IgA, cell adhesion molecules, natural killer cell-mediated cytotoxicity, and complement and coagulation cascades were detected as pathways linked to hair loss. Studies have linked the deposition of C3 at the hair follicle to scarring alopecia such as lupus erythematous, pemphigus vulgaris, and lichen planopilaris [8,21]. However, there is no clear evidence of complement involved in the pathogenesis of AA, although several studies reported deposits of C3 and IgA in perifollicular and at the base of hair follicles [21].…”

“…Studies have linked the deposition of C3 at the hair follicle to scarring alopecia such as lupus erythematous, pemphigus vulgaris, and lichen planopilaris [8,21]. However, there is no clear evidence of complement involved in the pathogenesis of AA, although several studies reported deposits of C3 and IgA in perifollicular and at the base of hair follicles [21]. Furthermore, CD8 + T cells, NK cells, and mast cells were signi cantly increased in AA and CLE lesions compared to PSOR lesions, implying that these cells may contribute to hair loss.…”