چکیده (انگلیسی):

Physicians think of mast cells and IgE primarily in the context of allergic disorders, including fatal
anaphylaxis. This ‘bad side’ of mast cells and IgE is so well accepted that it can be difficult to think of
them in other contexts, particularly those in which they may have beneficial functions. However, there is
evidence that mast cells and IgE, as well as basophils (circulating granulocytes whose functions partially
overlap with those of mast cells), can contribute to host defense as components of adaptive type 2
immune responses to helminths, ticks and certain other parasites. Accordingly, allergies often are
conceptualized as “misdirected” type 2 immune responses, in which IgE antibodies are produced against
any of a diverse group of apparently harmless antigens, as well as against components of animal venoms.
Indeed, certain unfortunate patients who have become sensitized to venoms develop severe IgEassociated
allergic reactions, including fatal anaphylaxis, upon subsequent venom exposure. In this review,
we will describe evidence that mast cells can enhance innate resistance to reptile or arthropod
venoms during a first exposure to such venoms. We also will discuss findings indicating that, in mice
which survive an initial encounter with venom, acquired type 2 immune responses, IgE antibodies, the
high affinity IgE receptor (Fc 3RI), and mast cells can contribute to acquired resistance to the lethal effects
of both honeybee venom and Russell's viper venom. These findings support the hypothesis that mast
cells and IgE can help protect the host against venoms and perhaps other noxious substances.