H-2-linked murine factor B phenotypes
- 1 January 1983
- journal article
- research article
- Published by Springer Nature in Immunogenetics
- Vol. 17 (1) , 67-78
- https://doi.org/10.1007/bf00364290
Abstract
A hemolytic assay has been developed which is specific for Factor B (B) activity in murine EDTA-plasma. Three discrete levels of B activity were observed among B 10-congenic strains. Mice with standard H-2 haplotypes, b, d, k, r, f, q, s, and u, all exhibited the same mean level of activity. However, plasma from H-2 v (B10.SM) mice contained only 0.25 of that level, and those with standard haplotype H-2 ja (B10.WB) or wild haplotype H-2wr7 (B10.WR) exhibited 2.5 times the H-2 b (1310) basal level of activity. These differences among B10 congenic lines suggested that the activity is H-2 controlled; further tentative mapping with intra-H-2 recombinants indicated that the gene is located in the S region. A fourth phenotype was found among progeny of backcross generations between B10.BR (H-2 k ) and mice of subspecies Mus musculus molossinus and M. m. bactrianus. This ultra-high activity was found also to be governed by a gene very closely linked to Ss, the primary S region marker. F1 generations between disparate phenotypes yielded progeny with activity levels intermediate between the parents; progeny of parents of different strains with the same phenotype expressed B hemolytic titres equal to those of the parental strains. No differences in antigenic levels of the protein among the strains of different phenotypes could be detected by radial immunodiffusion. In mixing experiments, resultant activity levels were intermediate between the higher and the lower phenotype, ruling out independent inhibitors or activators of the reaction. These studies indicate that an H-2-linked S region-located single gene governs structural differences in allelic B molecules that lead to differences in specific activities.This publication has 42 references indexed in Scilit:
- An autosomal dominant gene regulates the extent of 9-O-acetylation of murine erythrocyte sialic acids. A probable explanation for the variation in capacity to activate the human alternate complement pathway.The Journal of Experimental Medicine, 1980
- A murine C4 molecule with reduced hemolytic efficiency.The Journal of Experimental Medicine, 1980
- Interaction of beta1H globulin with cell-bound C3b: quantitative analysis of binding and influence of alternative pathway components on binding.The Journal of Experimental Medicine, 1978
- Human complement C3b inactivator: isolation, characterization, and demonstration of an absolute requirement for the serum protein beta1H for cleavage of C3b and C4b in solution.The Journal of Experimental Medicine, 1977
- Modulation of the alternative complement pathways by beta 1 H globulin.The Journal of Experimental Medicine, 1976
- On the Localization of the Gb Locus within the MHS Region of Chromosome No. 6Tissue Antigens, 1975
- Linkage of HL‐A and GBG1Vox Sanguinis, 1974
- C3 PROACTIVATOR CONVERTASE AND ITS MODE OF ACTIONThe Journal of Experimental Medicine, 1972
- SEROLOGICAL ANALYSIS OF A RECOMBINATION IN THE H-2 REGION OF THE MOUSETransplantation, 1966
- THE USE OF PVP AS A DEVELOPING AGENT IN MOUSE HEMAGGLUTINATION TESTSPlastic and Reconstructive Surgery, 1961