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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Nat Med. 2012 Sep;18(9):1401–1406. doi: 10.1038/nm.2862

Figure 1. IgG1 immune complexes (IC) inhibit C5a-mediated inflammatory responses in vivo and in vitro by an FcγRIIB-dependent mechanism.

Figure 1

Peritoneal migration of neutrophils in response to C5a (a) or OVA/anti-OVA-IC (b) ± 107.3-IC in WT, Fcer1g−/− or Fcgr2b−/−mice. Impact of 107.3-IC on (c) CD11b expression and (d) iC3b-dependent adhesion in neutrophils from Fcer1g−/− and Fcgr2b−/− mice. C5a-mediated migration of BM-derived neutrophils (e) and increase in [Ca2+]i in BM-derived cells (f) in WT, Fcer1g−/− or Fcgr2b−/− mice ± 107.3-IC. (g) Gating of BM neutrophils according to their FSC/SSC pattern (left dot-plot) and the expression of the Gr-1 marker (1st histogram on the left). Dose-dependent impact of 107.3-IC on C5a-mediated ERK1/2 phosphorylation in Gr-1+ WT BM neutrophils. (h) Effect of a C5a receptor antagonist (C5aRA) on C5a-mediated ERK1/2 phosphorylation. White histogram: ERK phosphorylation in the absence of C5a (background); grey histogram: treatment with C5a (5 × 10−7M; 1 min); magenta histogram: C5a (5 × 10−7M; 1 min) ± 107.3 IC (g) or C5aRA (h) at the indicated concentrations. Results in (c) and (g) are representative of at least three independent experiments. Values in (a) and (b), and (d-f) are means ± s.e.m. (n=5-10/group). *P<0.05, **P<0.01, ***P<0.001.