Open Access Research article

Autoantibody-mediated arthritis in the absence of C3 and activating Fcγ receptors: C5 is activated by the coagulation cascade

Jennifer L Auger1, Stefanie Haasken1,2 and Bryce A Binstadt1*

1 Center for Immunology and Department of Pediatrics, University of Minnesota, 2101 6th Street SE, Minneapolis, MN 55414, USA

2 Current address: Iowa Inflammation Program, University of Iowa, 2501 Crosspark Road, D168-MTF, Coralville, IA 52241, USA

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Arthritis Research & Therapy 2012, 14:R269 doi:10.1186/ar4117

Published: 13 December 2012

Additional files

Additional file 1:

IgG and C3 deposition in ankles of K/BxN mice lacking C3 or C5 and lacking FcR©. Deposition of IgG (red, left panels) and C3 (green, right panels) was determined by immunofluorescent microscopy in K/BxN mice expressing or not expressing C3, FcR©, and C5, as indicated in the left column. The key findings are that IgG is deposited in each of the joints. As expected, C3 is absent in the C3-deficient animal (A, lower right panel). Despite having decreased arthritis severity, C3 is still detectable in the joints of the C5/FcR©-deficient mouse (B, lower right panel). Slides were counterstained with DAPI (blue) to detect nuclei. Original objective: 40x.

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Additional file 2:

Hepatic expression of prothrombin/thrombin is upregulated in C3-deficient mice. Liver sections from C3-sufficient (left panels) and C3-deficient (right panels) mice were stained with monoclonal antibodies specific for prothrombin/thrombin (top panels) or isotype control antibodies (bottom panels). Brown staining represents bound antibody. The slides were counterstained with hematoxylin (blue). Original objective: 40x.

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