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A new review points to immunoglobulin E (IgE) as a potential central player in the overlapping mechanisms of psoriasis and atherosclerosis.
Researchers writing in Biomedicine and Pharmacotherapy proposed IgE-mediated mast cell (MC) activation as a significant contributor to the progression of both conditions and marking it as a therapeutic target.
Psoriasis and atherosclerosis, according to the study, share the pathophysiology of the IL-17-IgE axis, increasing immune responses in both diseases. Elevated serum IgE levels and increased mast cell presence in affected tissues have been observed in individuals with these comorbidities. The authors explained that IL-17A, a key cytokine in psoriasis, drives B-cell class switching to IgE production, activating mast cells via FcεRI receptors and releasing pro-inflammatory mediators. In psoriasis, these events exacerbate skin inflammation, while in atherosclerosis, they promote plaque instability and vascular damage.
The authors noted that while IL-17 inhibitors such as secukinumab have shown promise for psoriasis, options targeting IgE remain limited.
"Given the established role of IL-17 in this comorbidity, it is plausible that IgE could present a new therapeutic target for psoriasis patients with additional comorbidities," the researchers wrote in the study. "The activation of MCs appears to occur through the antigen-specific IgE aggregation at FcεRI receptors on their surface, a mechanism that warrants further validation in the context of psoriasis and atherosclerosis comorbidity. Future studies should also incorporate underexplored IL-17-related molecules or cell populations, including IgE and MCs, which have traditionally been overlooked in cell-mediated immunity. Such research has the potential to uncover valuable diagnostic biomarkers and identify new therapeutic targets."
Source: Wang Y, et al. Biomedicine and Pharmacotherapy. 2025. Doi:10.1016/j.biopha.2025.117860