BACKGROUND: Type I interferon (IFN) signature has been implicated in alopecia areata (AA). However, type I IFN source has never been documented. Plasmacytoid dendritic cells (PDCs) are generally known to be the main source and most potent producers of local type I IFNs. Their role in AA pathogenesis has never been investigated. OBJECTIVE: Investigate PDC role in AA. METHODS: Nineteen AA cases were retrieved from our database and were immunohistochemically tested for PDC occurrence and activity using anti-BDCA-2 and anti-MxA antibodies respectively. Comparison to 10 trichotillomania and 7 androgenetic alopecia (AGA) cases was also done. RESULTS: Plasmacytoid dendritic cells were present in all AA cases in a peri-bulbar location and, as indirectly assessed by MxA expression, were in an active state producing type I IFNs. All trichotillomania cases showed the presence of PDCs, though significantly less abundant and in a different distribution (mainly superficial perivascular) than that in AA. PDC presence and MxA expression were absent in AGA. CONCLUSIONS: Plasmacytoid dendritic cells constitute a central component of the peribulbar infiltrate in AA suggesting a significant role in AA pathogenesis. Additionally, PDC distribution could help in microscopically differentiating AA from trichotillomania or AGA.
BACKGROUND: Type I interferon (IFN) signature has been implicated in alopecia areata (AA). However, type I IFN source has never been documented. Plasmacytoid dendritic cells (PDCs) are generally known to be the main source and most potent producers of local type I IFNs. Their role in AA pathogenesis has never been investigated. OBJECTIVE: Investigate PDC role in AA. METHODS: Nineteen AA cases were retrieved from our database and were immunohistochemically tested for PDC occurrence and activity using anti-BDCA-2 and anti-MxA antibodies respectively. Comparison to 10 trichotillomania and 7 androgenetic alopecia (AGA) cases was also done. RESULTS: Plasmacytoid dendritic cells were present in all AA cases in a peri-bulbar location and, as indirectly assessed by MxA expression, were in an active state producing type I IFNs. All trichotillomania cases showed the presence of PDCs, though significantly less abundant and in a different distribution (mainly superficial perivascular) than that in AA. PDC presence and MxA expression were absent in AGA. CONCLUSIONS: Plasmacytoid dendritic cells constitute a central component of the peribulbar infiltrate in AA suggesting a significant role in AA pathogenesis. Additionally, PDC distribution could help in microscopically differentiating AA from trichotillomania or AGA.