Complement receptor one (CR1) is a ligand for the rosetting of Plasmodium falciparum infected red cells with uninfected cells. Since CR1 exhibits three known polymorphisms, we studied European-Americans (n = 112) and African-Americans (n = 330) and Malians (n = 158) to determine if genetic differences existed in an area endemic for malaria that could offer a survival advantage. The frequencies of Knops blood group phenotypes McC(b+) and Sl(a−) were greatly increased in Africans vs Europeans. Although the frequency of McC(b+) was similar between Africans from the USA or Mali, the Sl(a−) phenotype was significantly higher in Mali (39% vs 65%, respectively). There was an increased frequency of the largest size (250 kD) of CR1 in Mali, but this did not differ significantly from the USA (P = 0.09). Both cohorts of Africans had higher expression of red cell CR1 than European-Americans but this showed little difference between the USA and Mali groups. Thus, the most important CR1 polymorphism relevant to rosetting of malaria infected cells appears to be the Knops blood group. Genes and Immunity (2000) 1, 325-329.
ALMOST A CENTURY AGO, the first red cell blood groups, as determined by human sera, were described. During the subsequent years, great progress was made in the recognition and grouping of relationships of various specificities. There currently are 276 discrete red cell antigens. While 61 remain to be classified, 215 of these antigens can be grouped into 23 distinct systems. In 12 of the systems there exists a null cell, which is totally devoid of any representative antigens for that system. The recognition of a link between these biologic factors and a person's susceptibility to a particular disease has encouraged in-depth analyses of the individuals with these unusual phenotypes.The discoveries of extracellular hair-like appendages of microorganisms called pili, fimbriae, or (later) adhesins, that are directly related to infectivity, and of the hemagglutinating properties of bacteria that express these extracellular appendages were the first findings related to the bacterial cell-eukaryotic cell interaction. The contribution of these early findings to the understanding of the pathogenesis of infection, however, was not recognized for a long time. Nevertheless, Escherichiu coli induced different hemagglutination patterns of both human and animal red cells, which indicated that microorganisms could detect a variety of cell types and, thus, a variety of tissue ligands.2 Further studies explored the interaction between bacterial cells and other types of cells, including yeast, plant cells, and cells of animal and human origin^.^-^ For example, E. coli carrying the type 1 fimbriae were found to attach to mannans and aggregate yeast cells.An advancement in the understanding of the pathogenic properties of organisms that cause urinary tract infections came with the use of human uroepithelial cells as targets for the binding of E. coli, Proteus mirubilis, Abbreviations: CR = complement receptor; DAF = decay-accelerating factor; Gal = galactose; GalNAc = N-acetyl-galactosamine; GPI = glycophosphatidylinositol; NeuAc = N-acetyl-neuraminic acid; RCA = regulators of complement activation; SCR(s) = short consensus repeat(s); S R region = serine-and threonine-rich domain.
Utilizing mouse monoclonal antibodies which recognize Rodgers 1 and Chido 1 epitopes carried on the C4A and C4B molecules, and heat-aggregated IgG to activate Cl, an immunoassay was developed for the quantitation of total C4 as well as C4A and C4B. Interassay variation was 12.4, 11.5 and 10.8%, respectively. The immunoassay was compared to the quantitation of total C4 by radial immunodiffusion by testing 103 random white controls and gave a Pearson’s product-moment correlation coefficient of 0.81. Three genetic total-C4-deficient individuals were nonreactive in all three assays. This activated assay is specific, reproducible, and superior to existing methods for the quantitation of C4A and C4B and detection of the heterozygous C4 null state.
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