3.2. CRIg-Fc treatment does not affect serum levels of anti-dsDNA
The presence of high levels of circulating anti-dsDNA antibodies are immunologic hallmarks of SLE. To determinwhether CRIg-Fc treatment alters systemic auto-antibody production, we evaluated serum levels of anti-dsDNA of two subclasses in mice that were 16 weeks of age. No significant differences were observed in anti-dsDNA IgM (p = 0.51) or anti-dsDNA IgG (p = 0.88) antibody serum levels between the CRIg-Fc treated and control mice (Figs. 2A/B) indicating overall autoimmune factors are not universally affected by CRIg treatment. This finding suggests that CRIg does not interfere with the development of autoimmunity but rather with the recruitment of effectors of tissue damage.
3.3. CRIg-Fc treatment does not affect serum levels of total IgG
Elevated levels of IgG occur during immune activation and this elevation is observed in SLE disease. To assess if CRIg treatment affects systemic IgG levels, serum was assayed by ELISA. No significant difference was measured between the control and CRIg-treated groups (p = 0.16) (Fig. 2C).
3.4. CRIg-Fc treatment increases systemic levels of C3
C3 is a major component of all three complement pathways and inflammation results in the cleavage of C3 upon activation. SLE patients will have increased complement consumption which results in decreased levels of a number of complement proteins derived from C3 activation. We measured C3 levels in the serum of 16-week old treated and untreated mice by ELISA and found that treatment with CRIg-Fc resulted in significantly higher levels of C3 (p = 0.029), indicating less C3 cleavage has occurred (Fig. 2D). Apparently, C3 is consumed locally in the skin and kidney