Immunoglobulin E (IgE) activates mast cells (MCs). It remains unknown whether IgE also activates other inflammatory cells, and contributes to the pathogenesis of abdominal aortic aneurysms (AAAs). This study demonstrates that CD4⁺ T cells express IgE receptor FcεR1, at much higher levels than do CD8⁺ T cells. IgE induces CD4⁺ T‐cell production of IL6 and IFN‐γ, but reduces their production of IL10. FcεR1 deficiency (Fcer1a^−/−) protects apolipoprotein E‐deficient (Apoe^−/−) mice from angiotensin‐II infusion‐induced AAAs and reduces plasma IL6 levels. Adoptive transfer of CD4⁺ T cells (but not CD8⁺ T cells), MCs, and macrophages from Apoe^−/− mice, but not those from Apoe^−/− Fcer1a^−/− mice, increases AAA size and plasma IL6 in Apoe^−/− Fcer1a^−/− recipient mice. Biweekly intravenous administration of an anti‐IgE monoclonal antibody ablated plasma IgE and reduced AAAs in Apoe^−/− mice. Patients with AAAs had significantly higher plasma IgE levels than those without AAAs. This study establishes an important role of IgE in AAA pathogenesis by activating CD4⁺ T cells, MCs, and macrophages and supports consideration of neutralizing plasma IgE in the therapeutics of human AAAs.