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,,
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Divisions of
*
Emergency Medicine and
Immunology, Children’s Hospital Medical Center, Cincinnati, OH 45229;
Division of Immunology, Department of Internal Medicine and
Department of Pediatrics, University of Cincinnati, College of Medicine, Cincinnati, OH 45267;
¶ Veterans Administration Medical Center, Cincinnati, OH 45220; and
|| Nutrient Requirements and Functions Laboratory, Beltsville Human Nutrition Research Center, U.S. Department of Agriculture, Beltsville, MD 20705
We evaluated whether IL-4, a cytokine critical for inducing allergic responses, also contributes to the effector phase of allergy. Pretreatment of mice with IL-4 or the related cytokine, IL-13, rapidly and dramatically increased the severity of anaphylaxis induced by cross-linking Fc
RI or Fc
RIII. This effect was inhibited by endogenously produced IFN-, was T cell-, B cell-, and common -chain-independent, and required IL-4R
and Stat6. IL-4R signaling also enhanced anaphylaxis in mice infected with a nematode parasite that stimulates IL-4/IL-13 production. IL-4 exacerbated anaphylaxis by acting synergistically with vasoactive mediators to increase vascular permeability. Synergy between IL-4 and vasoactive mediators during the effector phase of allergic inflammation may both contribute to allergic immunopathology and enhance protective immunity against gastrointestinal worms.
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