![]() ![]() In AA, most commonly affected area is the scalp. It is significant to understand both the pathomechanism of AA and responsible cytokines in order to develop new treatments for recalcitrant AA. Also, in another recent study, it was supported that Th1-type cytokine profile is related to disease activity of AA, whereas Th2-type cytokines may be associated with the persistence of AA. Besides, recently published studies investigating the cytokine profile in lesional AA scalp indicates concurrent activation of Th1 and Th2 immune axes, as well as interleukin (IL)-23 and IL-32 cytokine pathways. Interleukin (IL)-2 and IL-15 are well known drivers of cytotoxic activity by IFN-γ-producing CD8+ Tcells and natural killer (NK) cells. Cytotoxic CD8+ NKG2D+ T cells are key players in the pathogenesis of AA that produce interferon-γ (IFN-γ). Many genes that are found to be associated with AA are also related to the immune system. Evidence suggests that AA results from the loss of immune privilege with presentation of autoantigens, triggered by environmental factors in genetically susceptible individuals. This means that hair follicles are immune-protected sites With deficient major histocompability complex (MHC) expression. Hair follicle is a dynamic immune privileged “miniorgan” with unique immune and hormone microenvironments. It targets primarily hair follicles and characterized by dense peribulbar lymphocytic infiltrate. It is considered to be a complex genetic, immune-mediated disease. ĭespite its high prevalence, the exact cause and triggering factors of AA are still unknown. Although onset may occur at any age, 60% of new cases had their first diagnosis before 20 years age. It affects 0.1–0.2% of the general population and accounts for 0.7% to 3.8% of all patients attending to dermatology clinics. Herein, we will review shortly the current treatment options in recalcitrant alopecia areata based on recently published studies and then will focus on the recently developed broad-spectrum and targeted therapeutics.Īlopecia areata (AA) is a common immune-mediated disorder. Recent research on immunology of hair follicle and recent developments in immunopathogenesis, together with the shared pathways of the disease with other autoimmune disorders, led investigators to focus on novel therapies that target specific immunological pathways. ![]() There are only a few randomized controlled studies conducted on recalcitrant AA. The factors indicating a poor prognosis are the extent of hair loss at the presentation, long duration of the disease, and ophiasis pattern of hair loss. The disease unfortunately has an unpredictable course. Besides, none of them are approved by Food and Drug Administration (FDA). Although many therapeutic options currently exist in alopecia areata, none of them are curative or preventive. Alopecia totalis and universalis are often difficult to treat. It may be patchy (localized), involve the entire scalp (alopecia totalis) or entire body (alopecia universalis). Alopecia areata (AA) is a common and complex T-cell–mediated inflammatory disorder. ![]()
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