Suppressor of cytokine signaling-1 regulates acute inflammatory arthritis and T cell activation
J. Clin. Invest. Paul J. Egan, et al. 111:915 doi:10.1172/JCI16156 [Go to this article.]

Figure 6
Expression of β-gal reporter gene activity in synovial tissue cells from SOCS-1^–/– IFN-γ^–/– mice on day 7 of acute arthritis. Synovial tissue cells were isolated by collagenase and dispase digestion of dissected synovium and incubated with FDG for 4 hours. Cells were then stained for expression of phenotypic markers. (a) Cells were stained with CD45 and CD11b, and gated populations were analyzed by light scatter (top row) and β-gal reporter gene activity (bottom row). Cells were incubated in the presence (thin histogram) or absence (b histogram) of FDG for 4 hours, followed by staining with phenotypic markers. (b) Cytocentrifuge preparations of CD11b⁺ synovial cells, sorted by flow cytometry on the basis of β-gal activity (Diff-Quik stain; magnification ×400). Results shown are representative of three independent experiments. (c) Lack of reporter gene expression in resident peritoneal macrophages. Resident peritoneal cells from naive SOCS-1^–/– IFN-γ^–/– mice were stained for CD11b⁺ expression and β-gal activity. Cells were incubated in the presence (thin histogram) or absence (b histogram) of FDG for 4 hours. Results shown are gated for CD11b⁺ cells.