The emerging picture regarding the role of eosinophils in the immune response appears to be the following: IL-3 [in humans, (251)], and/or IL-1 [in the mouse system, (253)], then IL-5 and GM-CSF [which are secreted from activated T-cells at the inflammation sites or even from activated mast cells (346-348)] induce differentiation and proliferation of eosinophils in bone marrow. Other factors, such as PAF (303-309), C5a, soluble parasite products (259-261), or even IL-5 (139), serve as chemoattractants for eosinophils to the sites of allergic inflammation, usually around mucosal surfaces. Eosinophil survival and state of activation is enhanced by IL-5 (139). Eosinophils degranulate, thus releasing their toxic granule proteins by cross-linking Ig receptors, the most potent of which is sIgA, and the degranulation is enhanced by IL-5, IL-3, GM-CSF, and other factors or parasite products. Eosinophil degranulation can also be induced by complement, as well as PAF. The interplay of all these different mediators, and their effects on eosinophil function, is an integral part of the eosinophil's involvement in different disease conditions. Eosinophils appear to be involved in the pathophysiology of different diseases, in part, by releasing their toxic granule contents in tissues and causing tissue damage.
|Original language||English (US)|
|Number of pages||31|
|State||Published - 1992|