The macrophages of Fcgr1−/− mice were reported to produce less Tumor Necrosis Factor α in the presence of B. burgdorferi but an absence of opsonizing antibody [15], suggesting not only that in early infection B. burgdorferi bacteria could more easily evade phagocytosis in null mutant animals but also that they are less likely to elicit inflammation. This evidence concerns the gene TNF and infection.