Background
Type 2 cytokine-related (i.e., type 2) immune responses associated with development of antigen-specific Immunoglobulin E antibodies (IgE) can contribute to pathology in allergic diseases and to fatal anaphylaxis. However, recent findings in mice indicate that IgE also can enhance defense against honeybee venom.
Objective
We tested whether IgE antibodies, IgE-dependent effector mechanisms, and a local anaphylactic reaction to an unrelated antigen can enhance defense against Russell's viper venom (RVV) and determined whether such responses can be influenced by immunization protocol or mouse strain.
Methods
We compared the resistance of RVV-immunized wild-type, IgE-deficient, and Fcer1a-deficient mice following injection of a potentially lethal dose of RVV.
Results
A single prior exposure to RVV enhanced the ability of wild-type mice, but not mice lacking IgE or functional FcεRI, to survive challenge with a potentially lethal amount of RVV. Moreover, IgE-dependent local passive cutaneous anaphylaxis in response to challenge with an antigen not naturally present in RVV significantly enhanced resistance to the venom. Finally, we observed different effects on resistance to RVV or honeybee venoms in BALB/c versus C57BL/6 mice which had received a second exposure to that venom prior to challenge with a high dose of that venom.
Conclusion
These observations illustrate the potential benefit of IgE-dependent effector mechanisms in acquired host defense against venoms. The extent to which type 2 immune responses against venoms can decrease pathology associated with envenomation seems to be influenced by the type of venom, the frequency of venom exposure, and the genetic background of the host.