Role of dendritic cells and B cells in the skin of imiquimod (IMQ)-induced psoriasis-like mouse model

Background Psoriasis is a chronic inflammatory skin disease traditionally characterized by T cell-mediated immune responses. However, dendritic cells (DCs) and B cells also contribute to immune regulation in psoriasis. Their role in disease progression remains underexplored. Methods This study utilized an imiquimod (IMQ)-induced psoriasis-like mouse model to investigate DC and B cell dynamics at different stages of disease progression (day 3, day 5 and day 7). Skin lesions were evaluated using the Psoriasis Area and Severity Index (PASI) and histological analysis. Flow cytometry was performed to assess the expression of CD11c + MHCII + DCs and CD19 + CD38 + B cells, while gene expression analysis using reverse transcriptase polymerase chain reaction (RT-PCR) of CD11c, H2-Aa, B cell activating factor (BAFF), interleukin (IL)-10, IL-6 and CXCR5 was conducted to elucidate immune modulation within the psoriasis skin microenvironment. Results IMQ application induced progressive skin thickening, erythema and scaling, with PASI scores significantly increased at day 7 compared to controls ( p = 0.002), reflecting pronounced inflammation. Histological analysis revealed epidermal hyperplasia, hyperkeratosis and dermal immune cell infiltration. Skin CD11c + MHCII + DCs were significantly elevated at day 3 ( p < 0.01), corresponding with upregulation of CD11c and H2-Aa genes, while CD19 + CD38 + B cells expanded at later stages, peaking at day 7 ( p < 0.0001), associated with increased BAFF , IL-10 , IL-6 and CXCR5 expression. A reduction in circulating B cells was observed alongside increased skin infiltration, suggesting a possible redistribution associated with inflammation. Conclusion Early DC activation corresponded with the initiation phase of inflammation, while the later expansion of B cells appeared to coincide with sustained inflammatory activity and disease progression. The coordinated presence of DCs and B cells in the skin microenvironment may influence disease severity and pathogenesis, which could provide fundamental insights for future investigations into potential therapeutic strategies.