Macrophage activation and innate resistance to infection in SCID mice.
Resistance to infection against a variety of pathogens requires the co-ordinated interaction of both the innate and acquired immune responses. Mice bearing the SCID mutation are devoid of T and B cells but retain elements of the innate immune system including natural killer (NK) cells, macrophages, granulocytes and complement proteins. Using the SCID model we have identified a T cell independent mechanism of macrophage activation mediated by the secretion of IFN-gamma from NK cells. This process occurs in response to a variety of parasites and bacteria including Listeria monocytogenes, and is strictly regulated both in vitro and in vivo by cytokines such as IL-2 and IL-10. Here we discuss the mechanisms of NK cell activation and regulation and describe a new model of opportunistic infection in SCID mice with the AIDS related pathogen Cryptosporidium parvum.
Bancroft
G J
GJ
Department of Clinical Sciences, London School of Hygiene and Tropical Medicine, England.
Kelly
J P
JP
D000818:Animals; D007113:Immunity, Innate; D007371:Interferon-gamma / Q000096:biosynthesis; D007694:Killer Cells, Natural / Q000276:immunology; D008088:Listeriosis / Q000209:etiology / Q000276:immunology; D008262:Macrophage Activation / Q000276:immunology*; D051379:Mice; D016513:Mice, SCID / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
D007371:Interferon-gamma