scholarly journals Specific suppression of major histocompatibility complex class I and class II genes in astrocytes by brain-enriched gangliosides.

1993 ◽  
Vol 178 (4) ◽  
pp. 1357-1363 ◽  
Author(s):  
P T Massa
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Class Ii ◽  
Binding Activity ◽  
Inducible Expression ◽  
Class I ◽  
Mrna Levels ◽  
Major Histocompatibility ◽  
Ifn Gamma ◽  
Histocompatibility Complex

The effect of brain-enriched gangliosides on constitutive and cytokine-inducible expression of major histocompatibility complex (MHC) class I and II genes in cultured astrocytes was studied. Before treatment with gangliosides, astrocytes expressed constitutive MHC class I but not class II molecules, however, the expression of both MHC class I and II cell surface molecules on astrocytes was induced to high levels by interferon gamma (IFN-gamma). Constitutive and IFN-gamma-inducible expression of MHC class I and II molecules was suppressed by treatment of astrocytes with exogenous bovine brain gangliosides in a dose-dependent manner. Constitutive and induced MHC class I and II mRNA levels were also suppressed by gangliosides, indicating control through transcriptional mechanisms. This was consistent with the ability of gangliosides to suppress the binding activity of transcription factors, especially NF-kappa B-like binding activity, important for the expression of both MHC class I and II genes. These studies may be important for understanding mechanisms of central nervous system (CNS)-specific regulation of major histocompatibility molecules in neuroectodermal cells and the role of gangliosides in regulating MHC-restricted antiviral and autoimmune responses within the CNS.

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 Characterization of 100 extended major histocompatibility complex haplotypes in Indonesian cynomolgus macaques

2019 ◽  
Author(s):  
Cecilia G. Shortreed ◽  
Roger W. Wiseman ◽  
Julie A. Karl ◽  
Hailey E. Bussan ◽  
David A. Baker ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Macaca Fascicularis ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Breeding Colony ◽  
Allelic Variants ◽  
Histocompatibility Complex ◽  
Cynomolgus Macaques

AbstractMany medical advancements – including improvements to anti-rejection therapies in transplantation and vaccine development – rely on pre-clinical studies conducted in cynomolgus macaques (Macaca fascicularis). Major histocompatibility complex (MHC) class I and class II genes of cynomolgus macaques are orthologous to human leukocyte antigen complex (HLA) class I and class II genes, respectively. Both encode cell-surface proteins involved in cell recognition and rejection of non-host tissues. MHC class I and class II genes are highly polymorphic, so comprehensive genotyping requires the development of complete databases of allelic variants. Our group used PacBio circular consensus sequencing of full-length cDNA amplicons to characterize MHC class I and class II transcript sequences for a cohort of 295 Indonesian cynomolgus macaques (ICM) in a large, pedigreed breeding colony. These studies allowed us to expand the existing database of Macaca fascicularis (Mafa) alleles by identifying an additional 141 MHC class I and 61 class II transcript sequences. In addition, we defined co-segregating combinations of allelic variants as regional haplotypes for 70 Mafa-A, 78 Mafa-B and 45 Mafa-DRB gene clusters. Finally, we defined class I and class II transcripts that are associated with 100 extended MHC haplotypes in this breeding colony by combining our genotyping analyses with short tandem repeat (STR) patterns across the MHC region. Our sequencing analyses and haplotype definitions improve the utility of these ICM for transplantation studies as well as infectious disease and vaccine research.

scholarly journals Major Histocompatibility Complex (MHC) Genes and Disease Resistance in Fish

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 378 ◽  
Author(s):  
Yamaguchi ◽  
Dijkstra
Keyword(s):  
Major Histocompatibility Complex ◽  
Disease Resistance ◽  
Mhc Class I ◽  
Teleost Fish ◽  
Class Ii ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Mhc Polymorphism ◽  
Genomic Regions

Fascinating about classical major histocompatibility complex (MHC) molecules is their polymorphism. The present study is a review and discussion of the fish MHC situation. The basic pattern of MHC variation in fish is similar to mammals, with MHC class I versus class II, and polymorphic classical versus nonpolymorphic nonclassical. However, in many or all teleost fishes, important differences with mammalian or human MHC were observed: (1) The allelic/haplotype diversification levels of classical MHC class I tend to be much higher than in mammals and involve structural positions within but also outside the peptide binding groove; (2) Teleost fish classical MHC class I and class II loci are not linked. The present article summarizes previous studies that performed quantitative trait loci (QTL) analysis for mapping differences in teleost fish disease resistance, and discusses them from MHC point of view. Overall, those QTL studies suggest the possible importance of genomic regions including classical MHC class II and nonclassical MHC class I genes, whereas similar observations were not made for the genomic regions with the highly diversified classical MHC class I alleles. It must be concluded that despite decades of knowing MHC polymorphism in jawed vertebrate species including fish, firm conclusions (as opposed to appealing hypotheses) on the reasons for MHC polymorphism cannot be made, and that the types of polymorphism observed in fish may not be explained by disease-resistance models alone.

scholarly journals Binding of Human Cytomegalovirus US2 to Major Histocompatibility Complex Class I and II Proteins Is Not Sufficient for Their Degradation

2002 ◽  
Vol 76 (16) ◽  
pp. 8265-8275 ◽  
Author(s):  
Mathieu S. Chevalier ◽  
Gwynn M. Daniels ◽  
David C. Johnson
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Human Cytomegalovirus ◽  
Class Ii ◽  
Degradation Pathway ◽  
Class I ◽  
Chimeric Proteins ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
C Terminus

ABSTRACT Human cytomegalovirus (HCMV) glycoprotein US2 causes degradation of major histocompatibility complex (MHC) class I heavy-chain (HC), class II DR-α and DM-α proteins, and HFE, a nonclassical MHC protein. In US2-expressing cells, MHC proteins present in the endoplasmic reticulum (ER) are degraded by cytosolic proteasomes. It appears that US2 binding triggers a normal cellular pathway by which misfolded or aberrant proteins are translocated from the ER to cytoplasmic proteasomes. To better understand how US2 binds MHC proteins and causes their degradation, we constructed a panel of US2 mutants. Mutants truncated from the N terminus as far as residue 40 or from the C terminus to amino acid 140 could bind to class I and class II proteins. Nevertheless, mutants lacking just the cytosolic tail (residues 187 to 199) were unable to cause degradation of both class I and II proteins. Chimeric proteins were constructed in which US2 sequences were replaced with homologous sequences from US3, an HCMV glycoprotein that can also bind to class I and II proteins. One of these US2/US3 chimeras bound to class II but not to class I, and a second bound class I HC better than wild-type US2. Therefore, US2 residues involved in the binding to MHC class I differ subtly from those involved in binding to class II proteins. Moreover, our results demonstrate that the binding of US2 to class I and II proteins is not sufficient to cause degradation of MHC proteins. The cytosolic tail of US2 and certain US2 lumenal sequences, which are not involved in binding to MHC proteins, are required for degradation. Our results are consistent with the hypothesis that US2 couples MHC proteins to components of the ER degradation pathway, enormously increasing the rate of degradation of MHC proteins.

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