Increased infiltration of CD11 c+/CD123+ dendritic cell subsets and upregulation of TLR/IFN-α signaling participate in pathogenesis of oral lichen planus.

<bold>Objective: </bold>Investigation of dendritic cell (DC) subsets and expression patterns of Toll-like receptors (TLRs) was conducted to understand the pathogenesis in oral lichen planus (OLP).<bold>Study Design: </bold>Blood, OLP lesion, and control samples were collected. Four DC subsets (CD11c+CD123-myeloid DC1 [mDC1], CD141+mDC2, CD11c-CD123+plasmacytoid DC [pDC], and CD1a+CD207+Langerhans cells [LC]) were investigated via flow cytometry (FCM) and immunohistochemical staining. Expression patterns of TLRs and their downstream molecules were analyzed via quantitative real-time polymerase chain reaction and immunohistochemistry in situ.<bold>Results: </bold>Thirty-two samples were collected (9 controls and 23 OLP patients). FCM results found that the percentages of LC, mDC1, mDC2, and pDC in situ were 0.0119 ± 0.0251%, 0.0064 ± 0.0134%, 0.0005 ± 0.0011%, and 0.0022 ± 0.0019% in control mucosa, respectively. The mDC1 (0.0300 ± 0.0276%) and pDC (0.0204 ± 0.0186%) subsets were significantly increased in OLP lesions (P < .01). No marked differences were evident, when comparing all 4 DC subsets from blood, between control and OLP groups. Significant upregulation of TLR7, TLR8, and TLR9 were disclosed in OLP (P < .01), along with their downstream interferon-α (IFN-α) signaling molecules (IRF7 and IFN-α, P < .01).<bold>Conclusion: </bold>Our findings of increased infiltration of pDC and mDC1, along with upregulation of TLR/IFN-α signaling, provide valuable information for further understanding the immunity in OLP. [ABSTRACT FROM AUTHOR]