Jiawei Jingxie Yin attenuates psoriasis recurrence and is associated with reduced NF-κB activation and memory γδ T cells in a mouse model.

Psoriasis frequently relapses after treatment withdrawal, suggesting persistence of cutaneous immune memory. Jiawei Jingxie Yin (JWJXY) is clinically used for psoriasis, but its relapse-related immunologic effects remain insufficiently characterized. Imiquimod (IMQ)-induced psoriasis and an IMQ rechallenge recurrence model were established in BALB/c mice. JWJXY (8/16/32 g/kg) was administered orally for 7 consecutive days. Lesion severity was assessed using PASI scoring. Epidermal pathology was evaluated by H&E staining. Serum IL-1β, IL-6, IL-18 and CXCL1 were measured by enzyme-linked immunosorbent assay (ELISA) kit. Keratinocyte hyperproliferation markers (K6, K16, Ki67) and TCRγδ in skin were assessed by immunofluorescence. NF-κB pathway activation (NF-κB, p-NF-κB, IκBα, p-IκBα) was assessed by western blot. Memory γδ T cells (CD44 +TCRγδ+) were quantified by flow cytometry in the recurrence setting. JWJXY dose-dependently improved IMQ-induced lesions and reduced PASI scores, accompanied by reduced epidermal hyperplasia and decreased K6/K16/Ki67 expression. JWJXY lowered serum IL-1β, IL-6, IL-18 and CXCL1. NF-κB pathway activation markers were reduced, including decreased p-NF-κB and p-IκBα. In the recurrence model, JWJXY attenuated rechallenge-associated disease severity and reduced cutaneous TCRγδ signal and memory γδ T-cell frequency. JWJXY ameliorated IMQ-induced psoriasis and attenuated recurrence, with associated reductions in systemic inflammatory mediators, keratinocyte hyperproliferation markers, NF-κB activation markers, and γδ T-cell readouts. Because Th17 cells and cellular IL-17A sources were not directly quantified, IL-17-axis interpretations should be considered hypothesis-generating and require confirmation; formal toxicity testing (e.g., serum chemistry) is also needed in future work.