A major histocompatibility complex class I allele shared by two species of chimpanzee

Cooper, S; Ej, Adams; Rs, Wells; Cm, Walker; Parham, Peter

doi:10.1007/s002510050350

Cited by 39 publications

(32 citation statements)

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“…Lawlor et al 1988;Adams et al 2000), even though these two species have been separated for over 5 million years (approximately 25N generations), far in excess of the time required for all traces of trans-species polymorphism to be lost in neutral genes. In addition, there are MHC alleles which are identical across species; an MHC-C allele is shared by two species of chimpanzee, believed to have diverged over 2 million years ago (Cooper et al 1998). Such findings can be explained by balancing selection slowing down the rate at which old alleles were lost and replaced by new ones, thus maintaining old lineages of alleles far longer than expected under neutral conditions (Klein et al 1998).…”

Section: Hla Alleles Differ At Many Sites and Have Long Coalescence Tmentioning

confidence: 90%

How selection shapes variation of the human major histocompatibility complex: a review

Meyer

Thomson

2001

Annals of Human Genetics

307

247

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summaryThe nature of polymorphism and molecular sequence variation in the genes of the human major histocompatibility complex (MHC) provides strong support for the idea that these genes are under selection. With the understanding that selection shapes MHC variation new questions have become the focus of study. What is the mode of selection that accounts for MHC polymorphism? Is variation maintained by pathogen pressure or by reproductive mechanisms? Discerning between these requires drawing on information from studies on association between HLA genes and infectious diseases, reproductive success and mating preferences relative to HLA genotypes, and theoretical studies that compare the outcomes of different selection regimes. The pattern that has emerged suggests that several types of selection are plausible for the maintenance of HLA polymorphism.

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Section: Hla Alleles Differ At Many Sites and Have Long Coalescence Tmentioning

confidence: 90%

How selection shapes variation of the human major histocompatibility complex: a review

Meyer

Thomson

2001

Annals of Human Genetics

307

247

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“…previously demonstrated that chimpanzee CD94/NKG2 interacts with human HLA-E, noting the high degree of structural conservation in CD94, NKG2, and MHC-E among primates. In contrast to CD94/NKG2 and MHC-E, killer cell Ig-like receptors and their MHC class Ia ligands have diverged considerably among primates (41,44). It has been proposed that sequence similarity among HLA-E and E-like sequences, including Qa-1, has arisen through convergent evolution driven by strong positive selection (45).…”

Section: Discussionmentioning

confidence: 99%

Analysis of HLA-E Peptide-Binding Specificity and Contact Residues in Bound Peptide Required for Recognition by CD94/NKG2

Miller

Weber

Ibegbu

et al. 2003

The Journal of Immunology

123

122

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The MHC class Ib molecule HLA-E is the primary ligand for CD94/NKG2A-inhibitory receptors expressed on NK cells, and there is also evidence for TCR-mediated recognition of this molecule. HLA-E preferentially assembles with a homologous set of peptides derived from the leader sequence of class Ia molecules, but its capacity to bind and present other peptides remains to be fully explored. The peptide-binding motif of HLA-E was investigated by folding HLA-E in vitro in the presence of peptide libraries derived from a nonameric leader peptide sequence randomized at individual anchor positions. A high degree of selectivity was observed at four of five total anchor positions, with preference for amino acids present in HLA-E-binding peptides from class Ia leader sequences. Selectivity was also observed at the nonanchor P5 position, with preference for positively charged amino acids, suggesting that electrostatic interactions involving the P5 side chain may facilitate assembly of HLA-E peptide complexes. The observed HLA-E peptide-binding motif was strikingly similar to that previously identified for the murine class Ib molecule, Qa-1. Experiments with HLA-E tetramers bearing peptides substituted at nonanchor positions demonstrated that P5 and P8 are primary contact residues for interaction with CD94/NKG2 receptors. A conservative replacement of Arg for Lys at P5 completely abrogated binding to CD94/NKG2. Despite conservation of peptide-binding specificity in HLA-E and Qa-1, cross-species tetramer-staining experiments demonstrated that the interaction surfaces on CD94/NKG2 and the class Ib ligands have diverged between primates and rodents.

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“…In addition, both HLA-C variants are present in gorilla (Lawlor et al 1991) and bonobo (Cooper et al 1998). One might expect gibbons (the lesser apes) to be intermediate between Old World monkeys and the great apes, but a recent study (Abi-Rached et al 2010a) has shown that their MHC class I ligands to have pursued quite a different course of evolution.…”

Section: Hla-c Ligands and Kirs In Non-human Primatesmentioning

confidence: 99%

Comparative studies of placentation and immunology in non-human primates suggest a scenario for the evolution of deep trophoblast invasion and an explanation for human pregnancy disorders

Carter

2011

Reproduction

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Deep trophoblast invasion in the placental bed has been considered the hallmark of human pregnancy. It occurs by two routes, interstitial and endovascular, and results in transformation of the walls of the spiral arteries as they traverse the decidua and the inner third of the myometrium. Disturbances in this process are associated with reproductive disorders such preeclampsia. In contrast, trophoblast invasion in Old World monkeys occurs only by the endovascular route and seldom reaches the myometrium. Recently, it was shown that this pattern is maintained in gibbons, but that the human arrangement also occurs in chimpanzee and gorilla. There is an interesting parallel with results from placental immunology regarding the evolution of the major histocompatability complex class I antigen HLA-C and its cognate receptors. HLA-C is not present in Old World monkeys or gibbons. It emerged in the orangutan and became polymorphic in the lineage leading to gorilla, bonobo, chimpanzee, and human. Interaction between HLA-C1 and HLA-C2 on the surface of trophoblast and killer immunoglobulin-like receptors (KIRs) expressed by uterine natural killer cells are important regulators of trophoblast invasion. Evolution of this system in great apes may have been one prerequisite for deep trophoblast invasion but seems to have come at a price. The evidence now suggests that certain combinations of maternal genotype for KIRs and fetal genotype for HLA-C imply an increased risk of preeclampsia, fetal growth restriction, and recurrent abortion. The fetal genotype is in part derived from the father providing an explanation for the paternal contribution to reproductive disorders.

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A major histocompatibility complex class I allele shared by two species of chimpanzee

Cited by 39 publications

References 0 publications

How selection shapes variation of the human major histocompatibility complex: a review

How selection shapes variation of the human major histocompatibility complex: a review

Analysis of HLA-E Peptide-Binding Specificity and Contact Residues in Bound Peptide Required for Recognition by CD94/NKG2

Comparative studies of placentation and immunology in non-human primates suggest a scenario for the evolution of deep trophoblast invasion and an explanation for human pregnancy disorders

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