Several stimuli, including Ig receptors (especially for secretory IgA [sIgA] and IgG), as well as cytokines (IL-5, GM-CSF, and IL-3), activate the eosinophil. Cross-linking of the IgG receptor, FcγRII (CD32), enhances eosinophil survival, evidently by autocrine production of GM-CSF, and stimulates apoptosis of adherent eosinophils, through a β2-integrin-dependent mechanism. Secretory IgA is a very potent stimulus for eosinophil degranulation; its potency is mediated by the secretory component, which binds to the eosinophil and synergizes with cytokines or IgG for superoxide production. Eosinophil activation by cytokines and Igs is critically dependent on β2-integrins, especially Mac-1 (αMβ2). β2-Integrins participate in eosinophil superoxide anion production and in degranulation stimulated by TSLP, PAF, GM-CSF, cross-linking of FcγRII (CD32), sIgA, and IgG (Gleich 2000).
Activated eosinophils generate multiple cytokines (IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, IL-16,...
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References
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Roth N, Städler S, Lemann M, Hösli S, Simon HU, Simon D. Distinct eosinophil cytokine expression patterns in skin diseases – the possible existence of functionally different eosinophil subpopulations. Allergy. 2011;66:1477–86.
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Yousefi, S., Simon, HU. (2014). Eosinophil Activation. In: Mackay, I.R., Rose, N.R., Ledford, D.K., Lockey, R.F. (eds) Encyclopedia of Medical Immunology. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-9194-1_89
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