ReviewFrontiers in allergy2026
FcεRII (CD23) in dermatological disorders: structure, function, and clinical implications.
Review in Frontiers in allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
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0 citing papers in PubMed.
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FcεRII (CD23) is the low-affinity receptor for IgE with unique structural and functional properties that position it as both a regulator and an effector in type I hypersensitivity. Unlike FcεRI, CD23 is a type II C-type lectin that exists as membrane trimers (CD23a/CD23b) and as soluble fragments (sCD23) generated mainly by ADAM10. Through context-dependent mechanisms, including co-ligation with CD21 on B cells, oligomerization-dependent IgE binding, and interactions with integrins, CD23 can either suppress or amplify IgE synthesis, shape antigen presentation, and modulate downstream immune responses. Importantly, accumulating experimental and clinical evidence indicates that CD23 exerts a predominantly regulatory role in IgE homeostasis, although its soluble forms may contribute to amplification of inflammatory signaling in specific contexts. Emerging dermatologic data link CD23 to atopic dermatitis, chronic spontaneous urticaria, and bullous pemphigoid, where circulating soluble CD23 often correlates with total IgE and disease activity. This narrative review is based on a structured PubMed search (1980-2024) using predefined keywords related to CD23, IgE, and dermatological diseases. We synthesize current knowledge on CD23 structure and biology, its physiological and immunoregulatory roles, and disease-specific evidence in dermatology. We also discuss translational implications, including modulation of CD23 cleavage and anti-IgE strategies. Finally, we highlight key gaps that must be addressed to validate CD23 as a biomarker and therapeutic target in skin disease.
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