Fig 1: CARD9 deficiency effectively prevented PM-induced impairment in the recovery of blood flow and mechanical function of ischemic limbs, preserved capillary density and attenuated inflammatory infiltration in ischemic limbs. To determine the effect of CARD9 on the recovery of ischemic limb in mice with PM exposure, we performed animal experiment with age-matched CARD9 deficient (CARD9-/-) mice. As shown in (A), CARD9 knockout effectively prevented the PM-induced reduction of blood flow recovery (*p < 0.01 for WT-PM vs. CARD9-PM; #p < 0.01 for WT-PBS vs. WT-PM). In the meanwhile, CARD9 knockout partially, but significantly reversed the reduction of mechanical function in ischemic limbs in mice with PM exposure at days 14 and 21 [*p < 0.05, #p < 0.05; (B, C)]. Interestingly, there was no significant difference in the recovery of blood flow and mechanical function between CARD9 and WT mice with PBS treatment. Consistent with the recovery of blood flow and mechanical function, ex vivo histological analysis showed that CARD9 deficiency effectively prevented PM-induced decrease of CD31+ capillary density and attenuated inflammatory cell infiltration in ischemic limbs [*p < 0.01, #p < 0.01; (D–G)]. DAPI, 4,6-diamidino-2-phenylindole. Scale bar, 50 µm. n = 7/group. Statistical differences were determined with ANOVA followed by Tukey's post-hoc test.