The absence of TNF permits myeloid Arginase 1 expression in experimental L. monocytogenes infection.

During an immune response inflammatory macrophages with their wide variety of effector mechanisms including the expression of inducible nitric oxide synthase play an important part in the defense against invading pathogens. The inflammatory phenotype requires the presence of TNF which suppresses alternative activation. In the bacterial Listeria monocytogenes infection model inflammatory macrophages are crucial for protection. After infection, TNF-deficient hosts have a similar number of splenic macrophages but die rapidly. A more detailed analysis of these cells showed that while inducible nitric oxide synthase is expressed at a comparable level TNF-deficient macrophages show an increased expression of Arginase 1.