Limited recruitment of cytokine producing cells into the sites of infection may be a general principle in host-pathogen interactions and help pathogens escape the host response, as shown in a Leishmamia major mouse model of dermal infection60 and in Listeria monocytogenes-infected mice, where Ccl2-induced recruitment of TNF and iNOS producing cells to the spleen mediates an effective innate immune response61. This evidence concerns the gene CCL2 and infection.