Mast cells are important in the development of allergic and anaphylactic reactions, but also in acquired and innate immunity.
There is also increasing evidence that mast cells participate in inflammatory diseases, where they can be activated by non-allergic triggers,
such as neuropeptides and cytokines, often having synergistic effects as in the case of substance P (SP) and IL-33. Secretion of
vasoactive mediators, cytokines and proteinases contribute to the development of coronary artery disease (CAD), as well as to dietinduced
obesity and the metabolic syndrome. Mast cells may be able to orchestrate such different biological processes through their ability
to release pro-inflammatory mediators selectively without the degranulation typical of allergic reactions. Recent evidence suggests
that mitochondrial uncoupling protein 2 (UCP2) and mitochondrial translocation regulate mast cell degranulation, but not selective mediator
release. Better understanding of these two processes and how mast cells exert both immunostimulatory and immunosuppressive actions
could lead to the development of inhibitors of release of specific mediators with novel therapeutic applications.
Keywords: Coronary artery disease, diabetes, inflammation, mast cells, mitochondria secretion
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