In Ackr2-deficient mice, at all time points following infection, the population of macrophages, CD4+ and CD8+ lymphocytes, and other immune cells was considerably more significant in lungs and liver, leading to higher production of IL-1β, IFN-γ, CCL2, CCL3, CCL5, and TNF-α in the bronchoalveolar lavage of infected mice. This evidence concerns the gene CCL2 and infection.