Review Article

Modulation of Immune-Inflammatory Responses in Abdominal Aortic Aneurysm: Emerging Molecular Targets

Table 1

Treatment effects of different immune therapeutic targets on the AAA progression.

TargetTreatment effectAgentModelReference

Immune systemDecrease aortic dilatationImmunosuppressive agentsElastase-induced rat aneurysm[18]
TLR2Decrease chronic inflammation, vascular remodeling and AAA formationTLR2-neutralizing mAbAngII-induced mouse aneurysm[30]
TLR4Repress aneurysm recurrenceAlginate oligosaccharideAneurysm patients[31]
TLR4/MyD88Attenuates AAA formationTanshinone IIAElastase-induced rat aneurysm[32]
TLR4/JNKInhibit experimental AAA developmentRosiglitazoneAngII-induced mouse aneurysm[33]
CXCR4Suppress AAA formation and progressionAMD3100CaCl2-induced mouse aneurysm[50]
CCR2 monocytesDecrease aortic dilatationEverolimusAngiotensin II- (A2-) infused apolipoprotein E-deficient mouse[58]
Complement alternative pathwayPrevent aneurysm formationProperdin-free AP C3 convertaseElastase-induced mouse aneurysm[62]
M1/M2 macrophages polarizationInhibit AAA formationD-series resolvinsElastase-induced mouse aneurysm[70]
Foxp3(+) TregsDecrease incidence (52%) and mortality (17%) of AAAInterleukin-2 complexApolipoprotein E-deficient mice fed a high-cholesterol diet with angiotensin II[110]
B cellsPrevent experimental AAA formationAnti-CD20 antibodyElastase perfusion or angiotensin II infusion apolipoprotein E-knockout mouse[128]
Mast cellsNo difference with the placebo groupPemirolastMedium-sized AAA patient[139]
NeutrophilsInhibit experimental AAA formationAntineutrophil antibodyElastase-induced mouse aneurysm[11]
NETsAttenuate AAA formationCl-amidine, an inhibitor NET formationElastase-induced mouse aneurysm[146]