We therefore hypothesized that high fat feeding may alter the accumulation and function of ILC2 systemically, and observed the ILC2 populations in the bone marrow (BM), spleen and peripheral lymph nodes of low-density lipoprotein receptor-deficient (Ldlr−/−) mice, a second atherosclerosis-susceptible strain, that had been maintained on HFD for 8 weeks. Here, LDLR is linked to atherosclerosis.