scholarly journals Major Histocompatibility Complex (MHC) Class I and MHC Class II Proteins: Conformational Plasticity in Antigen Presentation

2017 ◽  
Vol 8 ◽  
Author(s):  
Marek Wieczorek ◽  
Esam T. Abualrous ◽  
Jana Sticht ◽  
Miguel Álvaro-Benito ◽  
Sebastian Stolzenberg ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Antigen Presentation ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Conformational Plasticity

scholarly journals Major histocompatibility complex (MHC) fragment numbers alone – in Atlantic cod and in general - do not represent functional variability

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 963 ◽  
Author(s):  
Johannes M. Dijkstra ◽  
Unni Grimholt
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Fish Species ◽  
Teleost Fish ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Speciation Rates

This correspondence concerns a publication by Malmstrøm et al. in Nature Genetics in October 2016. Malmstrøm et al. made an important contribution to fish phylogeny research by using low-coverage genome sequencing for comparison of 66 teleost (modern bony) fish species, with 64 of those 66 belonging to the species-rich clade Neoteleostei, and with 27 of those 64 belonging to the order Gadiformes. For these 66 species, Malmstrøm et al. estimated numbers of genes belonging to the major histocompatibility complex (MHC) class I lineages U and Z and concluded that in teleost fish these combined numbers are positively associated with, and a driving factor of, the rates of establishment of new fish species (speciation rates). They also claimed that functional genes for the MHC class II system molecules MHC IIA, MHC IIB, CD4 and CD74 were lost in early Gadiformes. Our main criticisms are (1) that the authors did not provide sufficient evidence for presence or absence of intact functional MHC class I or MHC class II system genes, (2) that they did not discuss that an MHC subpopulation gene number alone is a very incomplete measure of MHC variance, and (3) that the MHC system is more likely to reduce speciation rates than to enhance them. We conclude that their new model of MHC class I evolution, reflected in their title “Evolution of the immune system influences speciation rates in teleost fish”, is unsubstantiated. In addition, we explain that their “pinpointing” of the functional loss of the MHC class II system and all the important MHC class II system genes to the onset of Gadiformes is preliminary, because they did not sufficiently investigate the species at the clade border.

A third broad lineage of major histocompatibility complex (MHC) class I in teleost fish; MHC class II linkage and processed genes

2007 ◽  
Vol 59 (4) ◽  
pp. 305-321 ◽  
Author(s):  
Johannes Martinus Dijkstra ◽  
Takayuki Katagiri ◽  
Kazuyoshi Hosomichi ◽  
Kazuyo Yanagiya ◽  
Hidetoshi Inoko ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Teleost Fish ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Processed Genes

scholarly journals Major histocompatibility complex (MHC) fragment numbers alone – in Atlantic cod and in general - do not represent functional variability

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 963
Author(s):  
Johannes M. Dijkstra ◽  
Unni Grimholt
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Fish Species ◽  
Teleost Fish ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Speciation Rates

This correspondence concerns a publication by Malmstrøm et al. in Nature Genetics in October 2016. Malmstrøm et al. made an important contribution to fish phylogeny research by using low-coverage genome sequencing for comparison of 66 teleost (modern bony) fish species, with 64 of those 66 belonging to the species-rich clade Neoteleostei, and with 27 of those 64 belonging to the order Gadiformes. For these 66 species, Malmstrøm et al. estimated numbers of genes belonging to the major histocompatibility complex (MHC) class I lineages U and Z and concluded that in teleost fish these combined numbers are positively associated with, and a driving factor of, the rates of establishment of new fish species (speciation rates). They also claimed that functional genes for the MHC class II system molecules MHC IIA, MHC IIB, CD4 and CD74 were lost in early Gadiformes. Our main criticisms are (1) that the authors did not provide sufficient evidence for presence or absence of intact functional MHC class I or MHC class II system genes, (2) that they did not discuss that an MHC subpopulation gene number alone is a very incomplete measure of MHC variance, and (3) that the MHC system is more likely to reduce speciation rates than to enhance them. Furthermore, their use of the Ornstein-Uhlenbeck model is a typical example of overly naïve use of that model system. In short, we conclude that their new model of MHC class I evolution, reflected in their title “Evolution of the immune system influences speciation rates in teleost fish”, is unsubstantiated, and that their “pinpointing” of the functional loss of the MHC class II system and all the important MHC class II system genes to the onset of Gadiformes is preliminary, because they did not sufficiently investigate the species at the clade border.

scholarly journals Major histocompatibility complex class II compatibility, but not class I, predicts mate choice in a bird with highly developed olfaction

2012 ◽  
Vol 279 (1746) ◽  
pp. 4457-4463 ◽  
Author(s):  
Maria Strandh ◽  
Helena Westerdahl ◽  
Mikael Pontarp ◽  
Björn Canbäck ◽  
Marie-Pierre Dubois ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Mate Choice ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class I ◽  
Allele Sharing ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
High Dependency

Mate choice for major histocompatibility complex (MHC) compatibility has been found in several taxa, although rarely in birds. MHC is a crucial component in adaptive immunity and by choosing an MHC-dissimilar partner, heterozygosity and potentially broad pathogen resistance is maximized in the offspring. The MHC genotype influences odour cues and preferences in mammals and fish and hence olfactory-based mate choice can occur. We tested whether blue petrels, Halobaena caerulea , choose partners based on MHC compatibility. This bird is long-lived, monogamous and can discriminate between individual odours using olfaction, which makes it exceptionally well suited for this analysis. We screened MHC class I and II B alleles in blue petrels using 454-pyrosequencing and quantified the phylogenetic, functional and allele-sharing similarity between individuals. Partners were functionally more dissimilar at the MHC class II B loci than expected from random mating ( p = 0.033), whereas there was no such difference at the MHC class I loci. Phylogenetic and non-sequence-based MHC allele-sharing measures detected no MHC dissimilarity between partners for either MHC class I or II B. Our study provides evidence of mate choice for MHC compatibility in a bird with a high dependency on odour cues, suggesting that MHC odour-mediated mate choice occurs in birds.

scholarly journals Fcγ Receptor–mediated Induction of Dendritic Cell Maturation and Major Histocompatibility Complex Class I–restricted Antigen Presentation after Immune Complex Internalization

1999 ◽  
Vol 189 (2) ◽  
pp. 371-380 ◽  
Author(s):  
Armelle Regnault ◽  
Danielle Lankar ◽  
Valérie Lacabanne ◽  
Ana Rodriguez ◽  
Clotilde Théry ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Antigen Presentation ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Antigen Processing ◽  
Class I ◽  
Peptide Transporter ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Dc Maturation

Dendritic cells (DCs) express several receptors for the Fc portion of immunoglobulin (Ig)G (FcγR), which mediate internalization of antigen–IgG complexes (immune complexes, ICs) and promote efficient major histocompatibility complex (MHC) class II–restricted antigen presentation. We now show that FcγRs have two additional specific attributes in murine DCs: the induction of DC maturation and the promotion of efficient MHC class I–restricted presentation of peptides from exogenous, IgG-complexed antigens. Both FcγR functions require the FcγR-associated γ chain. FcγR-mediated MHC class I–restricted antigen presentation is extremely sensitive and specific to immature DCs. It requires proteasomal degradation and is dependent on functional peptide transporter associated with antigen processing, TAP1-TAP2. By promoting DC maturation and presentation on both MHC class I and II molecules, ICs should efficiently sensitize DCs for priming of both CD4+ helper and CD8+ cytotoxic T lymphocytes in vivo.

scholarly journals Major histocompatibility complex (MHC) class II but not MHC class I molecules are required for efficient control ofStrongyloides venezuelensisinfection in mice

Immunology ◽  
2009 ◽  
Vol 128 (1pt2) ◽  
pp. e432-e441 ◽  
Author(s):  
Rosângela M. Rodrigues ◽  
Neide M. Silva ◽  
Ana Lúcia R. Gonçalves ◽  
Cristina R. Cardoso ◽  
Ronaldo Alves ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Efficient Control ◽  
Mhc Class I Molecules

Latent cytomegalovirus down-regulates major histocompatibility complex class II expression on myeloid progenitors

Blood ◽  
2002 ◽  
Vol 100 (8) ◽  
pp. 2867-2873 ◽  
Author(s):  
Barry Slobedman ◽  
Edward S. Mocarski ◽  
Ann M. Arvin ◽  
Elizabeth D. Mellins ◽  
Allison Abendroth
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Surface ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Latent Infection ◽  
Class Ii ◽  
Class I ◽  
Viral Gene ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

Following primary infection, human cytomegalovirus (CMV) establishes a lifelong latent infection in bone marrow–derived myeloid lineage cells. Although downmodulation of major histocompatibility complex (MHC) class I and class II protein levels occurs during active viral replication, little is known about the modulation of these proteins during latent infection. When analyzed by flow cytometry, latently infected adherent cells collected from granulocyte macrophage progenitor (GM-P) cultures exhibited a striking reduction in MHC class II antigen present on the cell surface starting very early after exposure to virus that continued for more than 2 weeks. In comparison, cell surface levels of the monocyte cell surface marker CD14 remained unaltered in these cells. A recombinant virus (RV798) lacking the virus genes US2-US11 retained the ability to downmodulate MHC class II levels during latent infection. Immunoblot and immunofluorescent antibody staining analyses showed that the reduction in MHC class II surface levels during latency was associated with a block in protein trafficking. HLA-DR was retained within cytoplasmic vesicles that also contained HLA-DM. Thus, downmodulation remained independent of all previously characterized MHC class I and class II immunomodulatory viral gene products and involved a mechanism not previously ascribed to any viral function. These data show that latent infection is accompanied by reduced cell surface expression of MHC class II proteins, a strategy that would afford the virus escape from immunosurveillance and increase the chances for lifelong latent infection.

scholarly journals A gene required for class II-restricted antigen presentation maps to the major histocompatibility complex.

1991 ◽  
Vol 174 (6) ◽  
pp. 1607-1615 ◽  
Author(s):  
E Mellins ◽  
S Kempin ◽  
L Smith ◽  
T Monji ◽  
D Pious
Keyword(s):  
Major Histocompatibility Complex ◽  
Antigen Presentation ◽  
Somatic Cell ◽  
Class Ii ◽  
Homozygous Deletion ◽  
Class I ◽  
Somatic Cell Hybrids ◽  
Major Histocompatibility ◽  
Cell Hybrids ◽  
Histocompatibility Complex

We have previously described a set of mutants (16.23-selected mutants) of a B lymphoblastoid cell line that are defective in the presentation of intact proteins to class II-restricted T cells, but effectively present immunogenic peptides. The mutations in these mutants are recessive in somatic cell hybrids and are not in Class II structural genes. Here, we report on a unique mutant, 5.2.4, in which a similar defect in class II-restricted antigen presentation has occurred in association with a one-megabase homozygous deletion in the class II region of the major histocompatibility complex (MHC). The defects in class II presentation among three of the 16.23-selected mutants, and between these mutants and 5.2.4, are noncomplementary in somatic cell hybrids. This suggests that the class II presentation-defective phenotype in all four mutants results from lesions in a single MHC-linked gene, a conclusion strengthened by the finding that in a hybrid made with a second, unrelated MHC deletion mutant, T2, the class II presentation defect in a 16.23-selected mutant is also not complemented. Mutant 5.2.4, in addition to its class II presentation defect, is also defective in surface expression of MHC class I molecules, most likely because its deletion encompasses the peptide supply factor 1 gene, whose function is known to be required for normal abundance of cell surface class I molecules. However, the surface abundance of class I molecules is normal in the 16.23-selected mutants, suggesting that the lesions affecting class I surface abundance and class II presentation result from mutations in different genes.

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