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Immunoglobulin E autoantibodies against interleukin-24 (IgE-anti-IL-24) are pathogenic autoantibodies that play a central role in the 'type IIb' (autoimmune) endotype of chronic spontaneous urticaria (CSU). Research indicates that IL-24 is a major autoantigen for IgE in a significant proportion of CSU patients (Schmetzer et al., 2018). These autoantibodies bind to the high-affinity IgE receptor (FcεRI) on mast cells and basophils; when they subsequently encounter endogenous IL-24, the resulting cross-linking triggers the release of histamine and other inflammatory mediators responsible for wheals and angioedema (Altrichter et al., 2021). From a therapeutic perspective, these antibodies are effectively neutralized by omalizumab, which sequesters free IgE and reduces the density of FcεRI receptors on effector cells. The presence and concentration of IgE-anti-IL-24 have been identified as valuable biomarkers for predicting a patient's response to anti-IgE therapy and for assessing disease severity (Schmetzer et al., 2018). Consequently, monitoring these autoantibodies allows for more precise patient stratification and personalized treatment approaches in chronic inflammatory skin conditions.
Neutralization of circulating free IgE-anti-IL-24, preventing its binding to the high-affinity IgE receptor (FcεRI) on mast cells and basophils, which in turn leads to the downregulation of these receptors and inhibition of mediator release (Maurer et al., 2013).
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