Mast cells are a critical first line of defense against endogenous and environmental threats. Their participation in innate immunity is well characterized; activation of
toll like receptors as well as receptors for
complement,
adenosine, and a host of other
ligands leads to mast cell release of preformed mediators contained within granules along with newly synthesized
arachidonic acid metabolites,
cytokines, and
chemokines. These confer protective effects including the induction of mucus secretion, smooth muscle contraction, and activation of common itch and
pain sensations, all of which act to promote expulsion of noxious agents. While their innate immune role as sentinel cells is well established, recent research has brought into focus their separate but also critical function in adaptive immunity particularly in the setting of
IgE mediated
food allergies. Crosslinking of FcεR1, the high affinity receptor for
IgE, when bound to
IgE and
antigen, triggers the release of the same factors and elicits the same physiologic responses that occur after activation by innate stimuli. Though
IgE-activated mast cells are best known for their role in acute
allergic reactions, including the most severe manifestation,
anaphylaxis, accumulating evidence has suggested an immunoregulatory effect in T cell-mediated immunity, modulating the balance between type 2 immunity and tolerance. In this review, we outline how mast cells act as adjuvants for food
antigen driven Th2 cell responses, while curtailing Treg function.