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. 2007 May 7;104(20):8433–8437. doi: 10.1073/pnas.0702936104

Fig. 4.

Fig. 4.

Activity of IgG-G0 antibodies in the K/BxN serum transfer model of arthritis. (A) The level of serum IgG sialylation in arthritic K/BxN mice compared with healthy wild-type controls was determined by lectin blotting with SNA and normalized to the loading control as described (14). (B) K/BxN serum was left untreated or treated with neuraminidase and galactosidase (K/BxN-SA-Gal) followed by isolation of serum IgG and determination of terminal galactose residues by blotting with ECL. The Coomassie-stained gel is shown as a loading control (load). (C and D) C57BL/6 or MBL-null (MBL 1/2) mice were injected with K/BxN serum either untreated (C) or pretreated with neuraminidase and galactosidase (K/BxN-SA-Gal) (D) and analyzed for the development of arthritis over the next 10 days; clinical scores were calculated as described in Materials and Methods. (E) C57BL/6 or common FcR γ-chain knockout mice (g−/−) were injected with untreated or neuraminidase- and galactosidase-treated serum and followed for the development of arthritis. (F) Ankle sections of C57BL/6, MBL-null, or FcR γ-chain knockout mice (γ−/−) that were injected with untreated K/BxN serum, serum depleted in sialic acid and galactose (K/BxN-SA-Gal), or PBS as a control were prepared at days 8–10 after serum injection and stained with H&E to detect the infiltration of inflammatory cells.