PubMed · 3562469
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H J Zeitz, T F Lint, A Gewurz, H Gewurz. 1986. Component deficiencies. 7. The seventh component.. https://pubmed.ncbi.nlm.nih.gov/3562469/
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C7 M/N typing, the determination of the allotypes of the recently described C7 M/N protein polymorphism, was conducted on serum samples from donors and recipients of 100 liver transplantations to determine whether the liver is the predominant site of in vivo synthesis of human complement protein C7. Twenty-one cases were informative as the recipient was transplanted with the liver obtained from a donor with a different C7 M/N allotype. The determination of the C7 levels and phenotypes of up to 10 post-transplantation (p.t.) samples revealed that there was at most only a 50% contribution of the transplanted liver toward the C7 M/N allotype at 2 to 3 wk p.t.; that influence decreased with time and was approximately 10% in the samples obtained later than 6 wk after transplantation. C7 is thus the only terminal complement component not predominantly synthesized by hepatocytes, which is compatible with the observation that C7 is not an acute phase reactant. The transient contribution of the donor phenotype appears to be attributable to cells of the mononuclear phagocyte lineage, Kupffer cells in particular that are replaced by cells of recipient origin. Various cells of that lineage that are known to synthesize C7 in vitro, therefore, contribute more toward the C7 concentration than previously anticipated. Enhanced local C7 synthesis at the site of inflammation might add further to the basic C7 level especially because C7 is often the limiting factor for terminal complement complex generation.
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The results of reference typing for C7 are presented and discussed. It appears that the present literature is using consistent nomenclature except that it was not possible to distinguish between the European C7-3 allele and Japanese C7-6. Oriental populations have both a higher frequency of variants and a greater variety of variants than Caucasian populations. Some samples with complex patterns defied classification, and it is speculated that these may be from persons with duplicated C7 genes. It is recommended that no change to the present system of nomenclature be made before a more detailed molecular understanding of the system is achieved.