Identification of Ss protein as murine C4

Abstract

DEMANT et al.¹ showed that the Ss-Slp region in the H–2 complex in mice affected the level of serum complement; the Ss high mouse having a higher complement activity than the Ss low mouse. They went on to show that antiserum to Ss protein could deplete complement activity from mouse serum, which has been confirmed in another laboratory². This was the first association described between complement and the principal histocompatibility locus. Further associations have since come to light. In the mouse, C3 levels are controlled in part by a gene in the H–2 region³ although the effect is not large. On the other hand, the ‘C5 deficiency gene’ in the mouse is not linked to H–2 (ref. 4). In man the allotypes of factor B show close linkage to HLA (ref. 5). C2 deficiency in man is also HLA linked in family studies⁶ and a marked linkage disequilibrium has been observed between the ‘C2 deficiency gene’ and the haplotype HLA10,W18. In the family described with C4 deficiency, HLA linkage has also been described⁷. The C3 allotypes in man, however, are not linked to HLA, nor is the ‘C3 deficiency gene’⁸. For guinea pigs, the ‘C4 deficiency gene’ is linked to the principal histocompatibility locus⁹. Démant et al.¹ showed that the Ss protein is likely to be a complement component, and in this communication we provide evidence that the Ss protein is the murine equivalent of the fourth component, C4.