These results suggest that the upregulation of CD80 and CD86 expression on DCs may be critical for augmenting pathogenic T cell immune responses and AAA formation following angiotensin II infusion, and that CTLA-4 overexpression potently blunts the angiotensin II-induced DC maturation and subsequent pathogenic T cell immune responses. The gene discussed is CTLA4; the disease is triple-A syndrome.