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Montjoye_et_al-2019-Allergy.pdf
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Abstract
(en) In chronic spontaneous urticaria (CSU), mast cell degranulation has a central role in the occurrence of wheals; however, the pathogenesis of CSU also involves other complex immune mechanisms such as autoimmunity, inflammation, and coagulation. There are several arguments to classify CSU as an autoimmune disease, at least in some patients. Indeed, patients with CSU were found to more frequently have another autoimmune disease than the general population.1 Moreover, subsequent work demonstrated that some autoantibodies such as IgG autoantibodies directed against the α subunit of the mast cell high‐affinity IgE receptor (FcεRIα)2 are more frequently detected in the CSU population than in healthy subjects and cause mast cell activation/degranulation. The presence of IgE autoantibodies directed against anti‐thyroid peroxidase3 in some CSU patients moreover suggests an “autoallergic” basis of disease in this subset. “Autoallergy,” classified as type 1 autoimmunity, is thought to involve the local production of self‐allergens against which specific IgE are directed, thus inducing mast activation/degranulation. More recently, Schmetzer et al detected IgE against IL‐24 in the sera of CSU patients directly correlated with CSU activity.4 They also showed that, in vitro, exogenous IL‐24 induced histamine release from human mast cells sensitized with IgE against IL‐24 from CSU patients, but not with IgE from healthy controls.4 To our knowledge, expression of IL‐24 in CSU has never been reported. [...]
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De Montjoye, L., Herman, A., Hendrickx, E., Cheou, P., Blanchetot, C., Hofman, E., Baeck, M., & Dumoutier, L. (2019). Increased expression of IL-24 in chronic spontaneous urticaria. Allergy, 74(9), 1811-1813. https://doi.org/10.1111/all.13832 (Original work published 2019)