Abstract
Mast cells (MCs) regulate chronic inflammation through a myriad of activating cell surface receptors. Dysregulation of MC activation through IgE-dependent and -independent mechanisms (ie cytokines, neuropeptides) contributes to allergic and non-allergic diseases. MC-targeting strategies have focused on neutralizing individual mediators or activating receptors which may be insufficient to broadly reduce MC activity. Molecules that dampen multiple pathways of MC activation, such as sialic acid-binding Ig-like lectins (Siglecs), represent novel therapeutic options for inflammatory diseases.
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