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. Author manuscript; available in PMC: 2009 Feb 1.

Published in final edited form as: J Neuroimmunol. 2008 Feb;194(1-2):70–82. doi: 10.1016/j.jneuroim.2007.11.018

Fig 1 — A: Primary CNS mixed glial cells were surface-stained with CD11b and intracellularly stained with anti-GFAP antibody. B: Primary CNS glial cells (passage 2) were challenged with live LCMV-Arm or UV-inactivated LCMV-Arm for 18-24 hours. As controls, cells were treated with medium, mouse recombinant TNF-α (TLR-independent), Pam2 (TLR2 ligand) and poly:IC (TLR3 ligand). The levels of MCP-1 and RANTES in the supernatants were measured by ELISA. One representative of at least five experiments is shown.

Fig 1 — A: Primary CNS mixed glial cells were surface-stained with CD11b and intracellularly stained with anti-GFAP antibody. B: Primary CNS glial cells (passage 2) were challenged with live LCMV-Arm or UV-inactivated LCMV-Arm for 18-24 hours. As controls, cells were treated with medium, mouse recombinant TNF-α (TLR-independent), Pam2 (TLR2 ligand) and poly:IC (TLR3 ligand). The levels of MCP-1 and RANTES in the supernatants were measured by ELISA. One representative of at least five experiments is shown.