Alopecia Areata: A Review of Disease Pathogenesis

F. Rajabi; L.A. Drake; M.M. Senna; N. Rezaei

Disclosures

The British Journal of Dermatology. 2018;179(5):1033-1048. 

In This Article

Treatment Strategies

Multiple treatment strategies have emerged in recent years aiming at immunological targets revealed by pathophysiological investigations (Table 3). So far none of the traditional immunosuppressants and newer targeted treatments have been able to establish long-lasting remission. This is attributed to the heterogeneous nature of the immune responses in AA, which cannot be targeted with a single agent,[193] and the lack of anagen induction in the resting (catagen and telogen) HFs following restoration of IP.[194]

A number of suggestions have been made regarding future therapies, such as induction of peripheral tolerance in T cells, re-establishment of IP via administration of immune guardians, targeting the neuroendocrine-immune system and utilizing MIF (Table 4, Figure 4).

Figure 4.

Treatment strategies in alopecia areata. Ab, antibody; Ag, antigen; APC, antigen-presenting cell; CRH, corticotropin-releasing hormone; IFN, interferon; IL, interleukin; IP, immune privilege; JAK, Janus kinase; Kv1·3, voltage-gated potassium channel; MIF, macrophage migration inhibitory factor; MSH, melanocyte-stimulating hormone; NGF, nerve growth factor; NK, natural killer; SOCS, suppressor of cytokine signalling; SP, substance P; TGF, transforming growth factor; TNF, tumour necrosis factor.

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