Journal
JOURNAL OF IMMUNOLOGY
Volume 170, Issue 7, Pages 3835-3842Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.170.7.3835
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Funding
- NIAID NIH HHS [R01 AI45766, K08 AI50006, R01 AI35987] Funding Source: Medline
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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 FcepsilonRI or FcgammaRIII. This effect was inhibited by endogenously produced IFN-gamma, was T cell-, B cell-, and common gamma-chain-independent, and required IL-4Ralpha and Stat6. IL-4Ralpha 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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