Elevated IgE Levels in Psoriasis: An Atypical Subtype with Th2 Dominance and Overlapping Features of Atopic...

This study aimed to investigate the potential impact of elevated IgE levels in psoriasis patients by exploring the responses of T cell subsets and B cell subsets, along with their associated cytokines.

Cytokine levels were measured using ELISA, and total IgE levels were measured using ELISPOT assay, along with PBMCs were collected for flow cytometry analysis to assess CD4⁺ T cell subsets (Th1, Th2, Th17) using their signature cytokines (IFN-γ, IL-4, IL-17A, respectively). Additionally, the expression of CD23 and CD19 on peripheral blood lymphocytes was measured to evaluate B cell responses.

Despite similar psoriasis area severity index (PASI) scores between the high-IgE psoriasis (H-PSO) and psoriasis vulgaris (PSO) groups, patients in the H-PSO group exhibited significantly higher peak pruritus numerical rating scale (NRS) scores. The elevated peripheral blood IgE levels in H-PSO patients were positively correlated with PASI scores, but not necessarily with peak pruritus NRS scores. Consistent with the elevation in IgE levels, Th2 cells and IL-4 cytokine levels were increased, along with the CD19⁺CD23⁺ cell population in H-PSO patients. Conversely, Th17 cells and associated IL-17A cytokine levels were more pronounced in H-PSO Conversely, the percentage of Th17 cells was significantly higher in H-PSO patients than in those with atopic dermatitis (AD), whereas IL-17A levels showed a similar trend that did not reach statistical significance; no significant differences were observed between H-PSO and PSO patients. The levels of Th1 cells and associated IFN-γ cytokines remained comparable not only between the two types of psoriasis but also between each psoriasis group and the AD group.

These findings suggest distinct immune profiles in psoriasis patients with elevated IgE levels, characterized by heightened Th2 responses and CD23⁺ B cell populations, as well as a prominent Th17 response, underscoring the complexity of immune dysregulation in psoriasis.