Complement factor H (CFH)
protein is an inhibitor of the alternative pathway of
complement (AP) both in the fluid phase and on the surface of host cells. Mouse and human
complement factor H-related (CFHR)
proteins also belong to the fH family of plasma
glycoproteins. The main goal of the current study was to compare the presence of
mRNA for two mCFHR
proteins in spontaneously developing
autoimmune diseases in mice such as
dense deposit disease (
DDD),
diabetes mellitus (DM), basal laminar deposits (BLD),
collagen antibody-induced arthrits (CAIA) and
systemic lupus erythematosus (SLE). Here we report for the first time that the CFHR-C
mRNA was universally absent in the liver from three strains of lupus-prone mice and in a diabetic-prone mouse strain. The
mRNA levels (pg/ng) for CFH and CFHR-B in MRL-lpr/lpr, at 9 wks and 23 wks were 707.2±44.4, 54.5±5.75 and 729±252.9, 74.04±22.76, respectively. The
mRNA levels for CFH and CFHR-B in NZB/NZW mice, at 9 wks and 54 wks were 579.9±23.8, 58.8±1.41 and 890.3±135.2, 63.30±9.2, respectively. CFHR-C
protein was absent in the circulation of MRL-lpr/lpr and NZB/NZW mice before and after the development of lupus. Similarly,
mRNA and
protein for CFHR-C was universally absent in liver and other organs and in the circulation of NOD mice before and after the development of DM. In contrast, the mRNAs for CFH, CFHR-B and CFHR-C were universally present in the liver from mice with and without
DDD, BLD and CAIA. The levels of
mRNA for CFHR-B in mice with and without BLD were ∼4 times higher than the mice with lupus. The complete absence of
mRNA for CFHR-C in lupus and diabetic-prone strains indicates that polymorphic variation within the mouse CFHR family exists and raises the possibility that such variation contributes to lupus and diabetic phenotypes.