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. 2008 Jul 29;84(4):1039–1046. doi: 10.1189/jlb.0408256

Fig. 4.

Fig. 4.

CD11c+ liver NK cells are expanded and activated during viral infection. (A) Mice were inoculated with 5 × 1010 particles of adenovirus via the lateral tail vein and killed at the indicated times. The absolute numbers of hepatic DC, CD11c+ NK cells, and CD11c NK cells were enumerated by flow cytometry. (B) The surface expression of costimulatory molecules and NK cell receptors is shown for hepatic DC, CD11c+ NK cells, and CD11c NK cells from animals infected with adenovirus 24 h prior. Each of the above is representative of a minimum of three separate experiments using pooled hepatic leukocytes of three mice per group. (C) A MLR was performed using stimulators isolated from the livers of mice infected with adenovirus 3 days earlier. These data are representative of two separate experiments. (D) CD11c+ and CD11c liver NK cells were purified from infected animals, pulsed with the OVA323–399 peptide, and assayed for their ability to cause the proliferation of antigen-specific, transgenic OTII CD4 T cells. (E) The ability of CD11c+ and CD11c liver NK cells, purified from mice, injected with normal saline (NS) or adenovirus 3 days prior was tested in a chromium release assay using YAC-1 lymphoma cells as targets. A 7.5:1 E:T ratio is shown. These data are representative of two separate experiments. *, P < 0.05.