Studies on the polymorphism of the fifth component of complement in laboratory mice.
The fifth component of complement C5, as well as C3, plays an important role in the inflammatory response. Since our previous studies have implicated polymorphism of C3 in disease pathogenesis, similar studies were undertaken on C5 using inbred and outbred laboratory mice. Consistent with previous findings, male mice were shown to have higher serum C5 concentrations than female mice. In male SJL/J mice, however, the serum concentration of C5 was significantly greater than in males of other strains. An immunofixation electrophoretic method was therefore developed to determine whether SJL/J mice had a different electrophoretic form of C5. The electrophoretic mobility of C5 in serum from SJL/J mice was similar to that in other strains. Some mice, including NOD/Lt, Quackenbush and ARC, had complete C5 deficiency. Southern blotting showed that C5 deficiency in these mice was associated with the same gene rearrangement found in other C5-deficient laboratory mice. No difference in the structure of the C5 gene was seen between SJL/J mice and other C5-sufficient inbred strains. In contrast, C5-sufficient Quackenbush and ARC outbred mice had a unique C5 RFLP pattern.[1]References
- Studies on the polymorphism of the fifth component of complement in laboratory mice. Lynch, D.M., Kay, P.H. Exp. Clin. Immunogenet. (1995) [Pubmed]
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