Eosinophils and eosinophil-associated diseases
Antigen-dependent activation of mast cells (MCs) occurs primarily through FcεRI, the high affinity receptor for IgE, which causes the release and generation of vasoactive and inflammatory mediators of allergic inflammation1. Understanding the mechanisms that control IgE dependent MC activation is critical to the development of small molecular weight inhibitors of MC responses and to understanding aberrant regulation.
It is currently understood that FcεRI aggregated by antigen coalesce within specialized microdomains of the plasma membrane (lipidrafts), and this causes the activation of Src family tyrosine kinases (SFKs), among which Lyn is the most critical for the initial stages of signaling elicitation.Activated Lyn then phosphorylates the β and γ chains of the FcεRI, which respectively leads to recruitment of Lyn andrecruitment/activation of spleen tyrosine kinase (Syk), an obligatory step for further propagation and divergence of signaling cascades leading to the release of bioactive mediators 3-5 .Targeting of these receptor-proximal signaling events is preferable since they are common to all antigen induced MC responses
Journal of Clinical Immunology and infectious diseases
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