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• W1937113397 abstract "This article introduces a series of reviews covering Co-evolution of lymphocyte receptors with MHC class I appearing in Volume 267 of Immunological Reviews. The basic mechanisms of innate immunity emerged in invertebrates, and were passed on to the vertebrates. On the other hand, adaptive immunity is exclusively found in vertebrates, as is the system of rearranging antigen-receptor genes of B and T lymphocytes that underlies adaptive immunity. During early vertebrate evolution, two genome-wide duplications occurred. One of these is evident in the genomes of all living vertebrates, but the other is specific to the jawed vertebrates (fish, amphibians, reptiles, birds, and mammals) and did not involve the jawless vertebrates (lamprey and hagfish). A consequence of this difference is that the B and T cells of jawless vertebrates have antigen receptors built from leucine-rich repeat modules, whereas their counterparts in the jawed vertebrates are an assemblage of immunoglobulin domains. For two such structurally divergent classes of protein to arrive at so similar a function is the consequence of convergent evolution. This phenomenon also figures in the more recent evolution of lymphocyte receptors that recognize major histocompatibility complex (MHC) class I, but are not the products of rearranging genes 1, 2. Because of the two genome-wide duplications, genes encoding MHC class I and class I-related proteins, such as the CD1 family members that present lipids to NKT cells, γδT cells, and αβT cells 3, 4, are present at four genomic locations, each on a different chromosome 5. This distribution implies that MHC class I-like proteins existed before the two genome-wide duplications. In contrast to class I, MHC class II genes are limited to a single chromosomal location, the MHC proper. This difference is consistent with MHC class II molecules being of more recent origin than MHC class I, an emergence that occurred after the two genome-wide duplications. Consistent with this historical sequence, the family of MHC class I and class I-like molecules is highly diversified in structure and function 4, whereas the family of MHC class II molecules is smaller, specialized, and circumscribed. Taking this dichotomy to the limit are Atlantic cod and some cod-like (gadoid) species of teleost 2, 6. In the genomes of these bony fish, there are no genes encoding MHC class II α chains, MHC class II β chains, or the invariant chain, and to cap it all, the CD4 gene is non-functional. Cod have thus dispensed with CD4 T cells and the pathway of antigen presentation mediated by MHC class II molecules. These drastic changes could not all have happened at once, but occurred gradually over time by a process of co-evolution in which these functionally interdependent genes were progressively inactivated or eliminated from the ancestral cod population. One possible cause of this outcome was an episode of selection against some aspect of MHC class II-mediated antigen presentation to CD4 T cells. Alternatively, a population bottleneck and chance fixation of inactivated alleles or deletion haplotypes by genetic drift could reach the same endpoint. The cod's co-evolution did not end with the extinction of its MHC class II genes. Accompanying that process was a massive expansion of the MHC class I gene family, to a size of more than 100 genes. Their encoded MHC class I proteins are of two types. A conventional type, predicted to load peptides from intracellular pathogens in exocytic compartments, and a novel type predicted to load peptides from extracellular pathogens in endocytic compartments. The novel subset of MHC class I molecules thus appears to have undergone convergent evolution, acquiring the antigen-presenting functions usually associated with MHC class II molecules 7. A comparison of living jawed vertebrates finds mammals to be exceptional in having proteins of the MHC class I pathway of antigen presentation encoded by genes in the middle of the MHC class II region, far away from the MHC class I genes 2, 5. In all other jawed vertebrates, these genes, which include those encoding the transporter associated with antigen processing (TAP), are closely linked to the MHC class I genes. This creates a genetic situation in which a TAP gene and an adjacent MHC class I gene can co-evolve functionally compatible polymorphisms, without them being susceptible to disruption by meiotic recombination. As a result of such co-evolution, the TAP variant encoded by an MHC haplotype works better with the neighboring MHC class I variant than it does with the allotypic variants encoded by other MHC haplotypes. The most vivid demonstration of this phenomenon is to be seen in the chicken. In these domesticated birds, the combination of TAP and MHC class I polymorphism determines the repertoire of peptides presented, the abundance of MHC at the cell surface, and gives rise to strong associations with infectious disease 5. A comparison of living jawed vertebrates also offers insight into the composition of the ‘primordial’ MHC that was present in the common ancestor of the living (but not necessarily the dead) jawed vertebrates. In addition to MHC class I and II, TAP, and proteasome genes, the primordial MHC is predicted to have included genes for NKp30 and its ligand, a member of the B7 family of costimulatory molecules. Present in almost all jawed vertebrate species, NKp30 is the oldest and phylogenetically most conserved NK cell receptor. The nature of its VJ type immunoglobulin domain raises the possibility that rearranging antigen-receptor genes originated with the NKp30 gene and its invasion by the RAG transposon. Many mammalian NK cell receptors are encoded by one of two genetic complexes situated on different chromosomes than the MHC. The natural killer complex (NKC) specifies receptors with lectin-like structure, and the leukocyte receptor complex (LRC) specifies immunoglobulin-like receptors. Genome comparisons point to elements of the MHC, NKC, and LRC, as well as the rearranging antigen-receptor genes, having once been part of an ancient ‘precursor immune complex’ 2. NKG2D is a prominent activating NK cell receptor that can also be a co-receptor for T cells. NKG2D is very conserved and also distinguished by the variety and polymorphism of its MHC class I-like ligands 8, 9. These ligands are not present on the surface of healthy cells, but expression is induced by the stress of infection or malignant transformation. In humans, the MIC and ULBP proteins are ligands for NKG2D. The class I region of the human MHC consists of duplicated genomic blocks of around 100 kb in length, each containing an MHC class I gene and a MIC gene. Thus, these two gene families jointly co-evolved on the human line. Only two of the MIC genes remain functional, but they both exhibit an extensive polymorphism that appears to have been selected. The family of six ULBP genes is on the long arm of chromosome 6, while the MHC is on the short arm. The gene content and gene sequences of the MIC and ULBP families vary considerably between species; mice have no MIC genes, for example, evidence for the rapid evolution of these ligands. NKG2D and NKG2D ligands are present only in marsupial and placental mammals. Does their absence from the egg-laying mammals mean that NKG2D and its ligands contributed to the mammalian transition from laying their eggs to viviparity? CD94:NKG2A is an NKC-encoded inhibitory NK cell receptor that in humans recognizes complexes of HLA-E and nonamer peptides cleaved from the leader peptide of other HLA class I heavy chains. This type of interaction is present in mice and possibly exists throughout the mammals. It provides a general mechanism for NK cells to monitor the quantity and quality of cellular synthesis of MHC class I 10. Complementing the broad specificity of CD94:NKG2A are the killer cell immunoglobulin-like receptors (KIR), which in recognizing epitopes carried by subsets of HLA-A, -B, and -C allotypes have narrower specificities, used only by a fraction of the human population. Although CD94:NKG2A and HLA-E are conserved, the KIR and their HLA-A, -B, and -C ligands are extraordinarily diverse 10. The KIR locus of the LRC is distinguished by the extent of its gene content diversity, also called gene copy number diversity. Illustrating the scope of this diversity, 70 different haplotypes, each containing between 4 and 20 KIR genes, were detected in an analysis of US and UK Caucasian families 11. Although diverse, the KIR locus is well organized around fixed framework KIR genes at the middle and end of the locus. In between, the framework genes are varied combinations of KIR genes that are not fixed. Underlying KIR haplotype diversity is unequal crossing over, mediated by intronic retroelements that facilitate DNA breaks. The abundance of these elements suggests that the KIR locus has actually evolved to increase the speed of its evolution 11. In addition to gene content variation, KIR haplotypes are also diversified by allelic polymorphism, which is substantial for around half of the KIR genes. Although the allelic polymorphism of KIR genes has numerous influences on KIR function and KIR association with disease, it remains largely ignored simply because a quick, simple, cheap, and robust method for typing KIR alleles has yet to be devised; an opportunity knocks 11. The two mouse KIR genes were excised from the LRC and moved to the X chromosome, where their function remains obscure. As far as we can tell, the mouse KIR are not NK cell receptors that recognize MHC class I. However, as a consequence of convergent evolution, mice have a system of NKC-encoded, lectin-like Ly49 receptors that recognize MHC class I 12. The extent to which the functional properties of human KIR and mouse Ly49 are similar is uncanny, but there are some significant differences. Unlike KIR interactions with MHC class I 10, the Ly49 interactions are generally indifferent to bound peptide and contact is made with a different site on the MHC class I surface. Because of their flexible stem, Ly49 molecules can bind to MHC class I ligands expressed on the same cell (cis-interaction) or a different cell (trans-interaction), whereas KIR can only manage the trans-interaction. Properties in common with KIR include a mix of inhibitory and activating receptors, and Ly49 haplotypes with a similar framework structure that vary both in gene content and allelic polymorphism. As for the KIR locus, unequal crossing over underlies the variation in gene content and is facilitated by an abundance of repeat elements in the Ly49 locus. Aside from other rodents, the only species that have an Ly49 family of receptors are the equids: horses, asses, and zebras 12. When immunologists first realized that T cells leaving the thymus were MHC restricted, the T cells were said to undergo thymic education. Later when the process was shown to be one of stringent selection, the term was dropped in favor of thymic selection. Education is now born again, but in the context of NK cell biology. NK cell responses are directed toward unhealthy cells for which the MHC class I expression has become abnormally low. In this situation, the NK cell seems to recognize the missing-self MHC class I. Such perception is achieved through the use of inhibitory NK cell receptors that bind to self MHC class I determinants, deliver inhibitory signals, and prevent the NK cell from attacking healthy cells. In this situation, there is an even balance between inhibitory and activating NK cell signaling. In contrast, NK cell interaction with an unhealthy cell that expresses a low level of MHC class I stimulates weaker inhibitory signals that are overcome by the activating signals. Consequently, the NK cell is activated and responds by either killing the unhealthy cells, secreting cytokines, or doing both of these. To respond in this manner to missing self, NK cells are educated to recognize what is the normal range of expression of self MHC class I. This is a lively and occasionally contentious field of investigation that has thrown up a variety of vying models and theories. In the context of mouse NK cell biology, Kadri et al. 13 provided a balanced synthesis that emphasizes the impermanence of an NK cell's education and how it can change in time according to the local environment of MHC class I. There is even hope here for a unifying theory of NK cell education. In considering the quality of the education given to human NK cells, Goodridge et al. 14 sought inspiration from an established and once unifying theory, namely Newton's Laws of Motion. From analysis of an extensive literature, they argue that education is not a one-hit process that permanently changes the qualitative state of an NK cell. Instead, they propose a dynamic and continually active process that is affected by every cell–cell interaction that an NK cell experiences as it circulates throughout the body. In this model, the NK cell uses every such contact to fine-tune its response to missing-self MHC class I. In other words, each contact with a potential target cell is an action to which the NK cell responds with an equal reaction. Neither human KIR nor mouse Ly49 genes are constitutively expressed by NK cells. Instead, they have a stochastic or probabilistic mode of expression by which NK cells express different combinations of KIR or Ly49 receptors. The three main inhibitory KIR recognize the Bw4 epitope of HLA-A and -B and the C1 and C2 epitopes of HLA-C. The functional KIR repertoire is determined by the interaction between the KIR and HLA class I phenotypes. Individual humans can have 1–3 of the HLA class I epitopes recognized and 1–3 of their cognate inhibitory KIR. Complementing the variation in KIR interactions with HLA-A, -B, and -C is the conserved interaction of CD94:NKG2A with HLA-E. In human populations, the phenotypic diversity of NK cells expressing inhibitory receptors for HLA class I vary over two orders of magnitude 15. Although numerous individuals lack particular NK cell receptors and/or HLA class I ligands, all human populations retain the full complement of ligands and receptors. This results from a co-evolution between KIR and HLA class I genes that are not linked, but segregate on different chromosomes. This genetic situation is at the opposite end of the spectrum from the close-linked, co-evolving TAP and MHC class I genes of the chicken 5. The upward face of the MHC class I molecule that engages αβT-cell receptors is the same face that engages KIR and CD94:NKG2A 10. The latter interactions are both dependent on bound peptide but in different ways. Engagement of CD94:NKG2A is specific for the peptide derived from MHC class I leader sequences, as is the binding site of HLA-E. In contrast, the KIR interactions with MHC class I are described as being selective, because some, but not all, of the peptides bound to the class I permit KIR interaction. CD94:NKG2A and KIR have different sensitivities in detecting missing-self, which fits with KIR usually detecting the loss of a single MHC class I allotype, whereas CD94:NKG2A detects the aggregate loss of all the allotypes 16. The rhesus macaque (Macaca mulatta), a species of Old World monkey, is the most widely used non-human primate in biomedical research. It is also a species in which the origins of the human HLA and KIR systems can be glimpsed. Corresponding to the single human HLA-A and HLA-B genes are sizeable families of Mamu-A and Mamu-B genes in the rhesus macaque. Rhesus MHC haplotypes differ in their class I gene content, with some 5 Mamu-A and up to 19 Mamu-B genes being present. At residues 77–83 in the helix of the α1 domain, Mamu-A and Mamu-B have amino acid sequence motifs that correspond to the Bw4 and Bw6 epitopes defined by HLA serologists in the early 1960s. Bw4 also functions as a major ligand for human KIR, but Bw6 does not. As well as the canonical Bw4 and Bw6 motifs, Mamu-A and Mamu-B molecules have a variety of hybrid motifs, and the impression from the work to date is that many of these could be KIR ligands. Supporting such conjecture is the presence in the rhesus macaque KIR locus of 10–20 genes encoding KIR of phylogenetic lineage II, the lineage to which the two human KIR that recognize HLA-A and -B belong. The rhesus macaque exemplifies a general trend in the Old World monkeys that distinguishes them from all other primate species. Namely a co-evolution of MHC-A and -B with lineage II KIR drove a substantial increase in number of the genes encoding both the ligands and the receptors 17, 18. Old World monkeys do not have a gene corresponding to human HLA-C, nor do the gibbons, the lesser apes. In primate phylogeny, neither MHC-C gene is first seen in the orangutan, the Asian great ape. Although not fixed in orangutan, the emergence of MHC-C had a profound effect on the KIR locus in that species. The numerous lineage II KIR genes are reduced to a rump, and have been superseded by a modest expansion of genes encoding the phylogenetic lineage III KIR that recognize MHC-C. With fixation of MHC-C, the number of lineage III KIR genes is doubled, as seen in the chimpanzee KIR locus. Thus in the great apes, there has been a co-evolution of MHC-C with lineage III KIR that has increased their presence while reducing that of the lineage II KIR. In human evolution, structural reorganization of the KIR locus has created alternative A and B forms of KIR haplotype that are functionally distinct and correlate differently with a range of diseases and clinical syndromes. The A and B KIR haplotypes have clearly co-evolved, as indicated by their presence in all human populations, though varying in relative frequency 19. There is a case to be made that selective pressures from reproduction have played a significant role in the co-evolution of MHC-C and KIR in hominids (great apes and humans). During placentation, maternal NK cells cooperate with fetal trophoblast to remodel maternal arteries that will supply the placenta with blood through to term. This is a critical process because either an undersupply or oversupply of blood can have fatal consequences. Of the interactions between trophoblast ligands and maternal NK cell receptors, only those between trophoblast HLA-C and maternal HLA-C-specific KIR exhibit genetic variability. Pregnancies involving KIR A homozygous mothers and a fetus expressing paternal HLA-C with the C2 epitope tend to give smaller babies and are susceptible to miscarriage, pre-eclampsia, and low birth weight. Conversely, pregnancies involving KIR B homozygous mothers and a fetus expressing paternal HLA-C with the C2 epitope tend to give larger babies and are susceptible to birthing difficulties, notably obstructed labor. The complications and mortality associated with both these outcomes have been strong and persistent forces of selection that have put their mark on the immunogenetics of all human populations 20. The author has no conflicts of interest to declare." @default.
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• W1937113397 title "Co-evolution of lymphocyte receptors with MHC class I" @default.
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