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. 2019 Mar 26;19(5):4353–4363. doi: 10.3892/mmr.2019.10084

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 1. — TLR-4 mediates the expression of inflammatory cytokines in peritoneal macrophages from C3H/HeN mice induced by anti-β2GPI–IgG. C3H/HeN mice (TLR-4 intact; n=8 in each group) and C3H/HeJ mice (TLR-4 defective; n=8 in each group) were treated by intraperitoneal injection of NR-IgG (100 µg antibody per injection), anti-β2GPI–IgG (100 µg antibody per injection) at 0 and 48 h. Peritoneal macrophages were collected at 72 h after the first injection. Peritoneal macrophages in the positive control group were challenged with LPS (1 µg/g body-weight) 2 h before the experiment. The expression levels of inflammatory factors (TNF-α, IL-1β and IL-6) in peritoneal macrophages were detected by immunofluorescence with corresponding antibodies. The images are representative of three separated experiments with similar results. Magnification, ×400. TLR-4, Toll-like receptor-4; NR-IgG, isotype control antibody; anti-β2GPI, anti-β2-glycoprotein I; LPS, lipopolysaccharide; TNF-α, tumor necrosis factor-α; IL, interleukin.