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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: J Autoimmun. 2016 Jul 1;73:111–119. doi: 10.1016/j.jaut.2016.06.019

Figure 3. Anti-NC16A IgG4 inhibit binding and C.

Figure 3

′ fixation of anti-NC16A IgG1,3 at the BMZ in vitro.

Skin sections of NC16A mice were incubated with anti-NC16A IgG1,3 (1 μg/ml), IgG4 (0.25 μg/ml), or both IgG1,3 and IgG4 in the absence or presence of freshly prepared human serum (providing complete complement system). A. IgG binding. Anti-NC16A igG1,3, and 4 stained the BMZ. Pre- or co-incubation of anti-NC16A IgG4 but not control IgG4 with anti-NC16A IgG1,3 drastically reduced binding of anti-NC16A IgG1,3 at the BMZ as detected by FITC-conjugated IgG1-spefici secondary antibody (panel d). B. C′ fixation. In the presence of human serum, anti-NC16A IgG1,3 and not IgG4 fixed complement as determined by C3 deposition at the BMZ using FITC-conjugated human C3-specific secondary antibody. Pre- or co-incubation of anti-NC16A IgG4 but not control IgG4 with anti-NC16A IgG1,3 significantly inhibited C′ fixation by anti-NC16A IgG1,3 (panel d).