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. 2006 Mar 20;203(3):553–561. doi: 10.1084/jem.20052438

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Copyright © 2006, The Rockefeller University Press

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Figure 1. — MyD88 deficiency protected against generation and deposition of pathogenic IgG2a and 2b autoantibodies and SLE. (A) IgG subclass analysis of autoantibodies in the serum of 5-mo-old wt.B6 (n = 4), FcγRIIB^−/−MyD88^+/−.B6 (n = 8), and FcγRIIB^−/−MyD88^−/−.B6 (n = 6) mice. Shown are anti-DNA and antinuclear antigen titers as determined by ANA ELISA. IgG2a_b (haplotype: _b) and 2b autoantibodies were up-regulated in FcγRIIB^−/−MyD88^+/−.B6 mice compared with wt.B6 mice (P = 0.02 and P = 0.004, respectively), whereas IgG2a and 2b titers were reduced to baseline in the absent of MyD88 (P = 0.02 and 0.004, respectively). Horizontal bars represent the average. (B) Histological and immunofluorescence analysis of kidney sections of 9.5-mo-old mice stained with hematoxylin and eosin (H+E) or with anti–mouse IgG subclasses. Compared with the FcγRIIB^−/−MyD88^+/−.B6 mice, FcγRIIB^−/− MyD88^−/−.B6 mice showed no IgG2a_b and 2b immune complex deposition and pathology in the kidney. (C) Kidney sections in B were costained with anti–mouse IgG2b and anti-FcγRIV (reference 20) or with Mac-I. Sections are representative of three independent mice from each group. (D) Kaplan-Meier survival curves for FcγRIIB^−/−MyD88^+/+ or FcγRIIB^−/−.B6 mice.