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. Author manuscript; available in PMC: 2009 Sep 11.
Published in final edited form as: Nat Genet. 2008 May;40(5):553–559. doi: 10.1038/ng.137

Figure 1.

Figure 1

Nephrotoxic nephritis (NTN) and macrophage phenotypes in parental (WKY, Lewis) and chromosome 16 congenic strains (WKY.LCrgn2, LEW.WCrgn2). For NTN phenotypes, rats were killed 10 d after injection of nephrotoxic serum. (a–d) Glomerular crescents (a), fibrin deposition (b), macrophage infiltration defined by ED-1–positive cells per glomerular cross-section (c) and proteinuria (d), measured using at least four rats per strain. (e) Macrophage activation, assessed by Fc receptor mediated phagocytosis and oxidization. WKY, LEW and WKY.LCrgn2 BMDMs (three rats per strain) were stimulated with Fc oxyBURST. LEW and WKY.LCrgn2 BMDMs showed significantly less activation than WKY at all time points (P < 0.001; error bars, s.e.m.). (f) Sandwich ELISA for secretion of MCP-1 in basal (unstimulated) and LPS (100 ng/ml)-stimulated BMDMs; secretion of IL-10 in LPS-stimulated (100 ng/ml) WKY, LEW and WKY.LCrgn2 BMDMs. *P < 0.05 and **P < 0.001 compared to WKY; error bars, s.e.m.