IL4 and triple-A syndrome: Both pro-inflammatory Th1 cells secreting IFN-γ and thereby increasing the MMP-2 and MMP-9 expression[11, 14] and anti-inflammatory Th2 cells secreting IL-4 and concomitantly increasing the expression of MMP-9 and MMP-12 seem to be involved in AAA development.[18, 39] However, Th1 cells are also linked to protection against the formation of AAA, since blocking of IFN-γ signalling pathways induced AAA formation in allografted aortas.[18]