Disruption of the cellular inflammatory response to Listeria monocytogenes infection in mice with disruptions in targeted genes

The results of this study to dissect the nature of the acquired immune response to infection with Listeria monocytogenes in mice with targetted gene disruptions show that successful resolution of disease requires the essential presence of alpha beta T cells and the capacity to elaborate gamma interferon. In the absence of either of these entities, mice experience increasingly severe hepatitis and tissue necrosis and de within a few days. The data from this study support the hypothesis that the protective process is the efficient replacement of neutrophils in lesions by longer-lived mononuclear phagocytes; alpha beta-T-cell-knockout mice died from progressive infection before neutrophil replacement could occur, whereas in gamma delta-T-cell-knockout mice this replacement process in the liver has previously been shown to be much slower. Ire the present study we attribute this delay to reduced production of the macrophage-attracting chemokine MCP-1 in the gamma delta-T-cell-knockout animals. These data further support the hypothesis that gamma delta T cells are important in controlling the inflammatory process rather than being essential to the expression of protection.