Properdin factor B and histocompatibility loci linked in the rhesus monkey

Ziegler, John B.; Alper, Chester A.; Balner, H.

doi:10.1038/254609a0

Cited by 71 publications

(36 citation statements)

References 11 publications

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“…In guinea pigs, the gene that determines deficiency of C4 is also linked to the MHR (6), as are the genes that control the electrophoretic variants of C4 and Bf, factor B of the properdin pathway (7). Similarly linked to the MHR are the allotypes of Bf in humans (8) and rhesus monkeys (9) and those of C2 (10) and C4 in humans (11). Furthermore, the genes of the inherited deficiences of C2 and C4 segregate in humans with the HLA system (12,13).…”

mentioning

confidence: 99%

Murine complement component 3: genetic variation and linkage to H-2.

Silva¹,

Hoecker²,

Day³

et al. 1978

Proc. Natl. Acad. Sci. U.S.A.

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Two electrophoretic variants of murine complement component 3 (C3) were detected by using high-voltage electrophoresis of fresh mouse serum in agarose gels. Most of the inbred strains tested were homozygous for the S allele (for the slow-migrating variant); only four out of 46 strains had the alternative F allele (fast variant). Pen-bred Swiss-Webster animals belonged to one of three phenotypes-S. F, or SF-and the genes responsible for this variation segregated in a strictly Mendelian manner. In three such crosses, with 52 offspring, C3 segregated with H-2 in 46 instances, corresponding to a recombination frequency of -0.12.

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mentioning

confidence: 99%

Murine complement component 3: genetic variation and linkage to H-2.

Silva¹,

Hoecker²,

Day³

et al. 1978

Proc. Natl. Acad. Sci. U.S.A.

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“…4, there are striking similarities among the genes associated with the MHC of the mouse and those of the two reviewed primate species. These similarities even extend to the analogy of genes in the murine S region, which are associated with the level of serum complement activity (46) and perhaps additional genes controlling murine C3 and C4 levels (47,48) with the HL-A-linked genes which regulate C2 deficiency (49) or the Bf loci which determine polymorphisms in properdin factor B (GBG) of the alternate complement pathway (35,41,42) . An initial report (42), which has not been confirmed, demonstrated close linkage ofthe genes controlling GBG polymorphism with the Lad regions in certain human families .…”

Section: Resultsmentioning

confidence: 99%

“…Ziegler et al . (35) have recently demonstrated the linkage of the structural genes for GBG of the rhesus monkey to the RhL-A complex. These investigators have positioned the Bf locus outside the SD loci and tentatively outside the Lad, and Ir-GL genes.…”

Section: Resultsmentioning

confidence: 99%

“…An initial report (42), which has not been confirmed, demonstrated close linkage ofthe genes controlling GBG polymorphism with the Lad regions in certain human families . In addition, the rhesus Bf locus has been provisionally mapped outside the SD, Ir-GL, and Lad, loci (35) .…”

Section: Resultsmentioning

confidence: 99%

“…Similar mapping of SD vs. Lad regions hold true for the canine histocompatibility complex (40) . In addition, the Bf genes coding for factor B of the properdin system are also linked to the RhL-A and HL-A complex although the precise localization ofthe Bflocus is only tentative (35,41,42) . A final point of similarity between the human and monkey histocompatibility systems is the localization of genes outside the SD region in the area of the Lad genes which code for a restricted class of alloantigens found primarily on B lymphocytes (31,43).…”

Section: Resultsmentioning

confidence: 99%

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Mapping of the immune response genes in the major histocompatibility complex of the Rhesus monkey.

Dorf¹,

Balner²,

Benacerraf³

1975

The Journal of Experimental Medicine

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Interest in the Ir genes of rheus monkeys stems from their phylogenetic relationship to man and the extensive data already available on the major histocompatibility complex of the monkey. At least two independent dominant H-linked Ir genes have been identified in the rhesus. These genes control the ability of monkeys to respond to the random linear copolymer of glutamyl alanine (GA), or the dinitrophenyl conjugate of glutamyl lysine (DNP-GL). These synthetic polymers can elicit weak delayed-type skin reactions and strong humoral responses in some monkeys. In a series of unrelated monkeys phenotyped for the serologically defined RhL-A specificities of both segregant series, there were no correlations between any RhL-A specificity and responder status to the GA or DNP-GL polymers. However, segregation analysis of 21 rhesus families sired by 3 fathers indicated the capacity of the offspring to form antibodies was associated with genes coded for in the RhL-A complex. In three monkeys, verified recombination within the RhL-A complex between the genes coding for the serologically defined determinants (SD loci) and the gene(s) controlling the lymphocyte-activating determinants (Lad loci) responsible for mixed lymphocyte reactivity was established. In two of these monkeys the immune response genes controlling the DNP-GL response segregated with the Lad genes, while in the third case the Ir-GL gene segregated with the SD loci, tentatively localizing the Ir-GL gene between the SD and Lad loci. In addition, we have shown that genetically distinct genes control responsiveness to DNP-GL and GA. These genes were separated by recombination, thus one monkey inherited the Lad, Ir-GL, and SD loci from one paternal haplotype and by crossing over inherited the gene controlling GA responsiveness from the other paternal haplotype. The fine structure mapping of the RhL-A gene complex is compared with the H-2 and HL-A gene complexes. Several striking similarities were noted.

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Treatment of Aphasia

Albert¹

1998

Arch Neurol

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Properdin factor B and histocompatibility loci linked in the rhesus monkey

Cited by 71 publications

References 11 publications

Murine complement component 3: genetic variation and linkage to H-2.

Murine complement component 3: genetic variation and linkage to H-2.

Mapping of the immune response genes in the major histocompatibility complex of the Rhesus monkey.

Treatment of Aphasia

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