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. 2001 Jul 16;194(2):181–188. doi: 10.1084/jem.194.2.181

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© 2001 The Rockefeller University Press

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Acute loss of resistance to T. gondii in LRG-47–deficient mice. The indicated strains were inoculated intraperitoneally with 20 cysts T. gondii, and their ability to restrict the infection was assessed. (A) Wild-type (n = 6) and LRG-47–deficient mice (n = 6) were monitored for their survival for 40 d. KO, knockout. (B) Peritoneal exudate cells from wild-type (WT; n = 3), IFN-γ–deficient (n = 3), and LRG-47–deficient mice (n = 4) were isolated at 5 d after infection, and the presence of intracellular T. gondii was determined microscopically. (C) Sera were isolated from wild-type (n = 2) and LRG-47–deficient mice (n = 4) at 5 d after infection and used for IFN-γ and IL-12 determination by ELISA. A–C are representative results of two experiments.

Acute loss of resistance to T. gondii in LRG-47–deficient mice. The indicated strains were inoculated intraperitoneally with 20 cysts T. gondii, and their ability to restrict the infection was assessed. (A) Wild-type (n = 6) and LRG-47–deficient mice (n = 6) were monitored for their survival for 40 d. KO, knockout. (B) Peritoneal exudate cells from wild-type (WT; n = 3), IFN-γ–deficient (n = 3), and LRG-47–deficient mice (n = 4) were isolated at 5 d after infection, and the presence of intracellular T. gondii was determined microscopically. (C) Sera were isolated from wild-type (n = 2) and LRG-47–deficient mice (n = 4) at 5 d after infection and used for IFN-γ and IL-12 determination by ELISA. A–C are representative results of two experiments.