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. 2018 Jun 6;9:1183. doi: 10.3389/fimmu.2018.01183

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Copyright © 2018 Bartsch, Rahmöller, Mertes, Eiglmeier, Lorenz, Stoehr, Braumann, Lorenz, Winkler, Lilienthal, Petry, Hobusch, Steinhaus, Hess, Holecska, Schoen, Oefner, Leliavski, Blanchard and Ehlers.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Transfer of sialylated polyreactive IgG antibodies (Abs) derived from 56R^+/−Fcgr2b^−/− mice or administration of sialylated antigen-specific monoclonal IgG Abs reduces nephritis-induced mortality in Fcgr2b^−/− mice. (A–C) Transfer of sialylated polyreactive IgG Abs from 56R^+/−Fcgr2b^−/− mice reduces nephritis-induced mortality. (A) Graphical representation of the experimental strategy. Fcgr2b^−/− mice received ICs containing 100 µg of TNP-sheep IgG and 200 µg of either sialylated (native) or sialidase-treated de-sialylated (de-sial) polyreactive IgG Abs derived from 2–3-month-old 56R^+/−Fcgr2b^−/− mice. The positive control (pos. ctrl.) group was treated with PBS and TNP-sheep IgG only. After 14 days, nephritis was induced by injection of sheep IgG in CFA and subsequent intravenous injection of sheep anti-glomerular basement membrane nephrotoxic serum (NTS) 4 days later. (B) Fc sialylation of purified total serum IgG Abs from wt mice and purified polyreactive IgG Abs from 56R^+/−Fcgr2b^−/− mice before and after sialidase treatment was determined through EndoS-treatment and MALDI-TOF mass spectrometry (MS) (percentage of glycans with one or two sialic acid residues: S1 and S2; Figure S1 in Supplementary Material). (C) Kaplan-Meier survival analysis of the indicated groups. (D–F) Application of sialylated antigen-specific monoclonal IgG Abs reduces nephritis-induced mortality. (D) Graphical representation of the experimental strategy as described in (A). Fcgr2b^−/− mice were treated with ICs containing 100 µg of TNP-sheep IgG and 100 µg of either native non-sialylated (αTNP murine IgG1 non-sial) or in vitro sialylated (αTNP IgG1 +sial) monoclonal anti-TNP murine IgG1 (clone H5) Abs. After 14 days, nephritis was induced as described above. (E) Fc sialylation of the monoclonal anti-TNP murine IgG 1 Abs (clone H5) before and after in vitro sialylation was determined through EndoS-treatment and MALDI-TOF MS (the percentage of one or two sialic acid residues coupled to the glycan: S1, S2; Figure S1 in Supplementary Material). (F) Kaplan–Meier survival analysis for the indicated groups. One representative experiment out of two independent experiments is shown.