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Published online before print April 23, 2004
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/
T cells
Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia
1Correspondence: Department of Microbiology and Immunology, Emory University School of Medicine, 1510 Clifton Road, Atlanta, GA 30322. E-mail: ziegler{at}microbio.emory.edu
Evidence that 
/
T cells play a broad, immunoregulatory role has been accumulating steadily. We show here that myeloid cells are disregulated after peritoneal infection with Listeria monocytogenes in mice lacking / T cells. Inflammatory populations of neutrophils and monocytes recruited to the site of infection remained longer. Intracellular cytokine analysis showed that frequencies of myeloid cells producing interleukin-12 and tumor necrosis factor 
were higher and remained elevated longer after infection in mice genetically deficient in / T cells. In vivo dye-tracking studies indicated that the majority of inflammatory monocytes differentiated into resident tissue macrophages in situ. In vitro experiments confirmed that monocytes harvested from mice lacking / T cells were defective in their maturation process. This evidence suggests that / T cells promote differentiation in the monocyte/macrophage lineage. These cells are important for bactericidal activity, inflammatory cytokine production, clearance of inflammatory neutrophils, and ultimately, antigen presentation to T cells. Regulation of monocyte/macrophage differentiation may underlie a broad segment of the phenotypic alterations that have been reported in mice lacking / T cells.
Key Words: macrophages • monocytes • neutrophils • TNF • IL-12
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