Fig. 3

Batf KO inhibits CIA-induced synovitis, synovial hyperplasia, and angiogenesis. H&E staining (a) and scoring of synovial inflammation (n = 11) (b) in knee and ankle joints of nonimmunized (NI) and collagen-induced arthritis (CIA) wild-type (WT) and Batf^−/− (knockout (KO)) DBA/1 J mice. c Detection of cell proliferation by Ki67 staining in knee joint sections of NI and CIA WT and Batf^−/− DBA/1 J mice (n = 5). d Bromodeoxyuridine (BrdU) incorporation assays (n = 6) in FLS from WT and Batf^−/− DBA/1 J mice treated with vehicle or tumor necrosis factor (TNF)-α (100 ng/ml for 24 h). e Representative images (n = 6) of immunofluorescence microscopy of CD31, which was used to detect blood vessels in the ankle joints of NI and CIA WT and Batf^−/− DBA/1 J mice. f mRNA levels of the indicated molecules, as detected by RT-PCR in FLS isolated from NI synovium (n = 6). FLS were treated with or without the indicated concentrations of TNF-α or IL-6 (left), or with or without 400 MOI (multiplicity of infection) of empty adenovirus (Ad-C) or the indicated MOI of Ad-Batf (middle and right). BATF was also detected by Western blotting (middle). Lamin B was detected as a loading control. g WT and Batf KO FLS were treated with interleukin (IL)-6 or TNF-α. Indicated molecules were detected by RT-PCR (n > 5). Values are means ± SEM. Scale bars = 50 μm