Relevant bibliographies by topics / Major histocompatibility complex I (MHCI)

Academic literature on the topic 'Major histocompatibility complex I (MHCI)'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Major histocompatibility complex I (MHCI)"

1

Matte-Martone, Catherine, Jinli Liu, Dhanpat Jain, Jennifer McNiff, and Warren D. Shlomchik. "CD8+ but not CD4+ T cells require cognate interactions with target tissues to mediate GVHD across only minor H antigens, whereas both CD4+ and CD8+ T cells require direct leukemic contact to mediate GVL." Blood 111, no. 7 (April 1, 2008): 3884–92. http://dx.doi.org/10.1182/blood-2007-11-125294.

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Abstract Whether T-cell antigen receptors (TCR) on donor T cells require direct interactions with major histocompatibility complex class I or class II (MHCI/MHCII) molecules on target cells to mediate graft-versus-host disease (GVHD) and graft-versus-leukemia (GVL) is a fundamental question in allogeneic stem-cell transplantation (alloSCT). In MHC-mismatched mouse models, these contacts were not required for GVHD. However, this conclusion may not apply to MHC-matched, multiple minor histocompatibility antigen-mismatched alloSCT, the most common type performed clinically. To address this, we used wild-type (wt)→MHCI−/− or wt→MHCII−/− bone marrow chimeras as recipients in GVHD experiments. For GVL experiments, we used MHCI−/− or MHCII−/− chronic-phase CML cells created by expressing the BCR-ABL cDNA in bone marrow from MHCI−/− or MHCII−/− mice. TCR/MHCI contact was obligatory for both CD8-mediated GVHD and GVL. In contrast, CD4 cells induced GVHD in wt→MHCII−/− chimeras, whereas MHCII−/− mCP-CML was GVL-resistant. Donor CD4 cells infiltrated affected skin and bowel in wt→MHCII−/− recipients, indicating that they mediated GVHD by acting locally. Thus, CD4 cells use distinct effector mechanisms in GVHD and GVL: direct cytolytic action is required for GVL but not for GVHD. If these noncytolytic pathways can be inhibited, then GVHD might be ameliorated while preserving GVL.
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2

de la Calle, Claire M., Sarah A. Holzman, Umer Sheikh, Jonathan H. Huang, Haydn T. Kissick, Adeboya O. Osunkoya, Brian P. Pollack, Dattatraya Patil, Kenneth Ogan, and Viraj A. Master. "Evaluation of major histocompatibility complex class I expression in clear cell renal cell carcinoma as a prognostic tool." Journal of Clinical Oncology 33, no. 7_suppl (March 1, 2015): 469. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.469.

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469 Background: After nephrectomy for clear cell renal cell carcinoma (ccRCC) approximately one-third of patients develop metastases. Yet, with currently used prognostic tools such as the TNM staging and the Fuhrman nuclear grade (FNG) system, it is difficult to accurately assess prognosis for each patient. Here, we evaluated Major Histocompatibility Complex Class I (MHCI) expression as a potential prognostic immune marker in ccRCC. Methods: Fifty-five post-nephrectomy patients that presented with localized ccRCC were included. All patients had four or more years of follow up. MHCI was stained in the tumor sections via immunohistochemistry. Then, via an automated image analysis algorithm MHCI expression was quantitated with the Positivity score, the ratio of positively stained pixels over the total number of pixels. Results: Mean MHCI positivity score of the cohort was 0.75 (SE= ±0.20). At the end of the follow-up period, the patients who were alive had higher MHCI expression (0.80 positivity score; SE ±0.14) than those who died of disease (0.62 positivity score; SE= ±0.16; t test, p<0.0001). MHCI positivity scores above the mean were associated with increased cancer specific survival (Mantel-Cox, p=0.0021). MHCI expression was higher among patients with no recurrence (0.80; SE= ±0.16) compared to those that recurred during the study period (0.70; SE= ±0.22; t test, p=0.017); and time-to-recurrence was longer in patients with above mean MHCI positivity scores (Mantel-Cox, p=0.017). Patients who were alive with recurrence had increased MHCI expression (0.81; SE= ±0.10) compared to those who succumbed to disease recurrence (0.62; SE= ±0.25; t-test, p=0.0009). No correlation was detected between FNG and tumor expression of MHCI (ANOVA, p=0.655, F=0.423) or between stage at presentation and MHCI tumor expression (ANOVA, p=0.734, F=0.311). Conclusions: With an automated high-throughput image analysis, this cohort shows that increased MHCI expression in ccRCC is associated with improved prognosis after curative nephrectomy.
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3

Master, Viraj A., Sarah Holzman, Brian Pollack, and Adeboya O. Osunkoya. "Major histocompatibility complex class I (MHC 1) expression in clear cell renal cell carcinoma: Correlation with clinical outcome." Journal of Clinical Oncology 32, no. 4_suppl (February 1, 2014): 541. http://dx.doi.org/10.1200/jco.2014.32.4_suppl.541.

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541 Background: Most patients with clear cell renal cell carcinoma (ccRCC) initially present with localized disease but a fraction subsequently develop metastases. Current predictive models of ccRCC recurrence are imperfect, suggesting a need for additional predictors. Metastatic ccRCC may be modulated by the immune system, suggesting that the immune system plays a role in tumor progression. Major histocompatibility complex class I (MHC I) expression on tumor cells is critical for immune system recognition. Here, we analyzed MHC I expression in ccRCC and its correlation with clinical outcomes. Methods: ccRCC patients who underwent radical nephrectomy with a ≥4 years of follow-up, without T4 disease or metastasis at presentation were included. All slides were re-reviewed by a single Urologic Pathologist and blocks with tumor and adjacent renal parenchyma were selected for each case for immunohistochemical staining for MHC I . Whole slide scanning and automated image analysis was used; representative areas of tumor and normal kidney were selected and averaged with Aperio image analysis software (positive pixel count v. 9). Unpaired t-test and one-way ANOVA were performed in GraphPad Prism. Results: 34 patients were analyzed. Fuhrman nuclear grades (FNG) were: FNG 2 10/34 (29%), FNG 3 20/34 (59%) and FNG 4 4/34 (11%). Although there was no correlation with FNG and MHC1 (ANOVA, p=0.800), patients who were alive at follow up had increased MHCI expression (80.1% average positivity score) than those who died (53% average positivity score; t-test, p<0.0001). Patients living with recurrence had increased MHCI expression (81.3% positivity score) compared to those who succumbed to their disease (53.2% positivity score; t-test, p<0.0001). Conclusions: MHCI expression may be an important prognostic factor in ccRCC for recurrence free survival, and also for prognosis of those patients with recurrence. This is the first study to show that increased MHCI expression is a favorable prognostic indicator in metastatic ccRCC. These results suggest that MHCI expression plays an important role in tumor-host immune system interaction of ccRCC and merits further study.
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4

Holzman, Sarah A., Claire M. de la Calle, Haydn T. Kissick, Adeboye O. Osunkoya, Brian P. Pollack, Dattatraya Patil, Kenneth Ogan, and Viraj A. Master. "High Expression of Major Histocompatibility Complex Class I in Clear Cell Renal Cell Carcinoma Is Associated with Improved Prognosis." Urologia Internationalis 95, no. 1 (2015): 72–78. http://dx.doi.org/10.1159/000370164.

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Introduction: In this study we analyzed major histocompatibility complex class I (MHCI) expression as a potential prognostic immune marker for patients with clear cell renal cell carcinoma (ccRCC). Patients and Methods: 34 patients with localized ccRCC (pT1-pT3) who had undergone nephrectomy and had at least 4 years of clinical follow-up data were included in the study. Immunohistochemical staining for MHCI was performed on tumor sections. An automated image analysis algorithm was applied to representative tumor areas to quantitate the proportion of stained pixels (positivity score = positive pixels/total pixels) on scanned digital slides. Results: At the end of the study, the patients who were alive had increased MHCI expression (mean positivity score 0.80) compared to those who died of the disease (mean positivity score 0.53; p < 0.0001, t test). Patients who were alive with recurrence had increased MHCI expression (positivity score 0.81) compared to those who succumbed to their disease recurrence (positivity score 0.53; p < 0.0001, t test). Survival was higher among patients with high MHCI expression compared to patients with low MHCI expression (p < 0.0001, Mantel-Cox). Conclusions: With an automated high-throughput image analysis technique, this study shows that higher tumor cell MHCI expression promotes increased survival and reduced incidence of recurrence compared to patients with lower tumor cell MHCI expression.
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5

Mavridis, George, Richa Arya, Alexander Domnick, Jerome Zoidakis, Manousos Makridakis, Antonia Vlahou, Anastasia Mpakali, et al. "A systematic re-examination of processing of MHCI-bound antigenic peptide precursors by endoplasmic reticulum aminopeptidase 1." Journal of Biological Chemistry 295, no. 21 (March 17, 2020): 7193–210. http://dx.doi.org/10.1074/jbc.ra120.012976.

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Endoplasmic reticulum aminopeptidase 1 (ERAP1) trims antigenic peptide precursors to generate mature antigenic peptides for presentation by major histocompatibility complex class I (MHCI) molecules and regulates adaptive immune responses. ERAP1 has been proposed to trim peptide precursors both in solution and in preformed MHCI-peptide complexes, but which mode is more relevant to its biological function remains controversial. Here, we compared ERAP1-mediated trimming of antigenic peptide precursors in solution or when bound to three MHCI alleles, HLA-B*58, HLA-B*08, and HLA-A*02. For all MHCI-peptide combinations, peptide binding onto MHCI protected against ERAP1-mediated trimming. In only a single MHCI-peptide combination, trimming of an HLA-B*08-bound 12-mer progressed at a considerable rate, albeit still slower than in solution. Results from thermodynamic, kinetic, and computational analyses suggested that this 12-mer is highly labile and that apparent on-MHC trimming rates are always slower than that of MHCI-peptide dissociation. Both ERAP2 and leucine aminopeptidase, an enzyme unrelated to antigen processing, could trim this labile peptide from preformed MHCI complexes as efficiently as ERAP1. A pseudopeptide analogue with high affinity for both HLA-B*08 and the ERAP1 active site could not promote the formation of a ternary ERAP1/MHCI/peptide complex. Similarly, no interactions between ERAP1 and purified peptide-loading complex were detected in the absence or presence of a pseudopeptide trap. We conclude that MHCI binding protects peptides from ERAP1 degradation and that trimming in solution along with the dynamic nature of peptide binding to MHCI are sufficient to explain ERAP1 processing of antigenic peptide precursors.
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6

Lilley, Brendan N., Domenico Tortorella, and Hidde L. Ploegh. "Dislocation of a Type I Membrane Protein Requires Interactions between Membrane-spanning Segments within the Lipid Bilayer." Molecular Biology of the Cell 14, no. 9 (September 2003): 3690–98. http://dx.doi.org/10.1091/mbc.e03-03-0192.

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The human cytomegalovirus gene product US11 causes rapid degradation of class I major histocompatibility complex (MHCI) heavy chains by inducing their dislocation from the endoplasmic reticulum (ER) and subsequent degradation by the proteasome. This set of reactions resembles the endogenous cellular quality control pathway that removes misfolded or unassembled proteins from the ER. We show that the transmembrane domain (TMD) of US11 is essential for MHCI heavy chain dislocation, but dispensable for MHCI binding. A Gln residue at position 192 in the US11 TMD is crucial for the ubiquitination and degradation of MHCI heavy chains. Cells that express US11 TMD mutants allow formation of MHCI-β2m complexes, but their rate of egress from the ER is significantly impaired. Further mutagenesis data are consistent with the presence of an alpha-helical structure in the US11 TMD essential for MHCI heavy chain dislocation. The failure of US11 TMD mutants to catalyze dislocation is a unique instance in which a polar residue in the TMD of a type I membrane protein is required for that protein's function. Targeting of MHCI heavy chains for dislocation by US11 thus requires the formation of interhelical hydrogen bonds within the ER membrane.
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7

Weigert, Roberto, Albert Chi Yeung, Jean Li, and Julie G. Donaldson. "Rab22a Regulates the Recycling of Membrane Proteins Internalized Independently of Clathrin." Molecular Biology of the Cell 15, no. 8 (August 2004): 3758–70. http://dx.doi.org/10.1091/mbc.e04-04-0342.

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Plasma membrane proteins that are internalized independently of clathrin, such as major histocompatibility complex class I (MHCI), are internalized in vesicles that fuse with the early endosomes containing clathrin-derived cargo. From there, MHCI is either transported to the late endosome for degradation or is recycled back to the plasma membrane via tubular structures that lack clathrin-dependent recycling cargo, e.g., transferrin. Here, we show that the small GTPase Rab22a is associated with these tubular recycling intermediates containing MHCI. Expression of a dominant negative mutant of Rab22a or small interfering RNA-mediated depletion of Rab22a inhibited both formation of the recycling tubules and MHCI recycling. By contrast, cells expressing the constitutively active mutant of Rab22a exhibited prominent recycling tubules and accumulated vesicles at the periphery, but MHCI recycling was still blocked. These results suggest that Rab22a activation is required for tubule formation and Rab22a inactivation for final fusion of recycling membranes with the surface. The trafficking of transferrin was only modestly affected by these treatments. Dominant negative mutant of Rab11a also inhibited recycling of MHCI but not the formation of recycling tubules, suggesting that Rab22a and Rab11a might coordinate different steps of MHCI recycling.
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8

Clement, Mathew, Lea Knezevic, Tamsin Dockree, James E. McLaren, Kristin Ladell, Kelly L. Miners, Sian Llewellyn-Lacey, et al. "CD8 coreceptor-mediated focusing can reorder the agonist hierarchy of peptide ligands recognized via the T cell receptor." Proceedings of the National Academy of Sciences 118, no. 29 (July 16, 2021): e2019639118. http://dx.doi.org/10.1073/pnas.2019639118.

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CD8+ T cells are inherently cross-reactive and recognize numerous peptide antigens in the context of a given major histocompatibility complex class I (MHCI) molecule via the clonotypically expressed T cell receptor (TCR). The lineally expressed coreceptor CD8 interacts coordinately with MHCI at a distinct and largely invariant site to slow the TCR/peptide-MHCI (pMHCI) dissociation rate and enhance antigen sensitivity. However, this biological effect is not necessarily uniform, and theoretical models suggest that antigen sensitivity can be modulated in a differential manner by CD8. We used two intrinsically controlled systems to determine how the relationship between the TCR/pMHCI interaction and the pMHCI/CD8 interaction affects the functional sensitivity of antigen recognition. Our data show that modulation of the pMHCI/CD8 interaction can reorder the agonist hierarchy of peptide ligands across a spectrum of affinities for the TCR.
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9

Pommier, Arnaud, Naishitha Anaparthy, Nicoletta Memos, Z. Larkin Kelley, Alizée Gouronnec, Ran Yan, Cédric Auffray, et al. "Unresolved endoplasmic reticulum stress engenders immune-resistant, latent pancreatic cancer metastases." Science 360, no. 6394 (May 17, 2018): eaao4908. http://dx.doi.org/10.1126/science.aao4908.

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The majority of patients with pancreatic ductal adenocarcinoma (PDA) develop metastatic disease after resection of their primary tumor. We found that livers from patients and mice with PDA harbor single disseminated cancer cells (DCCs) lacking expression of cytokeratin 19 (CK19) and major histocompatibility complex class I (MHCI). We created a mouse model to determine how these DCCs develop. Intraportal injection of immunogenic PDA cells into preimmunized mice seeded livers only with single, nonreplicating DCCs that were CK19– and MHCI–. The DCCs exhibited an endoplasmic reticulum (ER) stress response but paradoxically lacked both inositol-requiring enzyme 1α activation and expression of the spliced form of transcription factor XBP1 (XBP1s). Inducible expression of XBP1s in DCCs, in combination with T cell depletion, stimulated the outgrowth of macrometastatic lesions that expressed CK19 and MHCI. Thus, unresolved ER stress enables DCCs to escape immunity and establish latent metastases.
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10

Parrish, Heather L., Neha R. Deshpande, Jelena Vasic, and Michael S. Kuhns. "Functional evidence for TCR-intrinsic specificity for MHCII." Proceedings of the National Academy of Sciences 113, no. 11 (February 1, 2016): 3000–3005. http://dx.doi.org/10.1073/pnas.1518499113.

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How T cells become restricted to binding antigenic peptides within class I or class II major histocompatibility complex molecules (pMHCI or pMHCII, respectively) via clonotypic T-cell receptors (TCRs) remains debated. During development, if TCR–pMHC interactions exceed an affinity threshold, a signal is generated that positively selects the thymocyte to become a mature CD4+ or CD8+ T cell that can recognize foreign peptides within MHCII or MHCI, respectively. But whether TCRs possess an intrinsic, subthreshold specificity for MHC that facilitates sampling of the peptides within MHC during positive selection or T-cell activation is undefined. Here we asked if increasing the frequency of lymphocyte-specific protein tyrosine kinase (Lck)-associated CD4 molecules in T-cell hybridomas would allow for the detection of subthreshold TCR–MHC interactions. The reactivity of 10 distinct TCRs was assessed in response to selecting and nonselecting MHCII bearing cognate, null, or “shaved” peptides with alanine substitutions at known TCR contact residues: Three of the TCRs were selected on MHCII and have defined peptide specificity, two were selected on MHCI and have a known pMHC specificity, and five were generated in vitro without defined selecting or cognate pMHC. Our central finding is that IL-2 was made when each TCR interacted with selecting or nonselecting MHCII presenting shaved peptides. These responses were abrogated by anti-CD4 antibodies and mutagenesis of CD4. They were also inhibited by anti-MHC antibodies that block TCR–MHCII interactions. We interpret these data as functional evidence for TCR-intrinsic specificity for MHCII.
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Dissertations / Theses on the topic "Major histocompatibility complex I (MHCI)"

1

Glithero, Ann. "Presentation of glycopeptides by major histocompatibility complex (MHC) class I." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267901.

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2

Godinez, Ricardo. "Comparative Genomics of the Major Histocompatibility Complex in Amniotes." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10685.

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The major histocompatibility complex region (MHC) is a multi gene family present in all jawed vertebrates, with a fundamental role in vertebrate immunity. More than two decades of studies have resulted in the characterization of over a dozen MHC regions, and models of evolution explaining that the MHC has gradually increased in size and gene content since its origins without addressing their genomic context or the environmental selective forces. Furthermore, a compelling reconstruction of the evolutionary history of the MHC has been hampered due to phylogenetic gaps and the absence of comparative phylogenetic methods applied to comparative genomics. Here I reconstruct 320 MY of MHC evolution using 42 amniote genomes using improved gene annotations, genomic alignments and phylogenetic algorithms to reconstruct the evolution of the MHC at three levels of phylogenetic resolution. The first one describes 25 MY of evolution of the primate MHC using eight Human and four non-Human primate MHC haplotypes. Results suggests that highly dense gene segments have a strikingly conserved gene organization, and six conserved and highly rearranging segments overlap genes that are most commonly associated to disease. Phylogenomic analysis implies that the MHC has remained stable in gene content and size, with significantly increased duplication rates in the primate ancestors. The second one describes 280 MY of MHC evolution through the first characterization of reptilian MHC region, which combines mammalian, reptilian, Bird and amphibian characteristics, which favors the hypothesis of the existence of a primordial MHC in which natural killer receptors, CD1 and lectin genes co-exist. The Anolis MHC expands our understanding of the origins of the exceptionally small Bird MHC regions and provides further information about the organization and size of the ancestral amniote MHC. The third one compares 42 amniote MHC regions and map gene duplications and losses to further evaluate the mode and tempo of the evolution of the region. Comparative phylogenetic methods imply that the genomic and environmental factors affect the diversification of MHC during 320 My of evolution.
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3

Qin, Jinyi. "Characterisation of the central region of the sheep major histocompatibility complex." Thesis, Curtin University, 2008. http://hdl.handle.net/20.500.11937/375.

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The major histocompatibility complex (MHC) is a chromosomal region encoding molecules controlling adaptive immune response in vertebrates. In farm animals, many associations between MHC loci and productivity traits including disease susceptibility have been described. However, current knowledge about the structure and function of the MHC in domestic animals, especially sheep, is very limited. Characterization of the sheep MHC may potentially facilitate breeding for enhanced disease-resistant animals through use of marker assisted selection. The main aim of this project has been to provide insights into the organization of the genomic content of the central region of the sheep MHC. The work described herein has utilized subcloning of a sheep BAC genomic library in conjunction with DNA sequencing to generate a map of the central region of the sheep MHC covering ≈700 kbp. Within this map the relative order and identity of twenty five recognized loci were established. For some loci the intergenic distances were also determined. The final map is the most accurate map of this region reported to date and shows a high degree of similarity to the analogous region of the human MHC. This work has been published and a copy of the paper is included in Appendix 1. During the course of this work detailed genomic sequences were obtained for several sheep central region loci. Complete nucleotide sequences were generated for the complement factor B locus (CFB) and the TNFα locus and a comparative analysis of these sequences confirmed their homology with other vertebrate orthologues. Extensive partial sequences for complement components C2 and C4 were also obtained and reported to GenBank.In addition, a previously identified short tandem repeat locus designated BfMs believed to be in the CFB locus was mapped to an intron within the adjacent SKI2VL locus. Single nucleotide polymorphisms (SNPs) were identified by analysing homologous sequences from a minimum of five individual sheep. In total 33 SNPs were discovered distributed over eleven distinct loci. Allele frequencies for SNPs from ten of these loci were determined and reported for a panel of 71 sheep comprising 58 unrelated sheep from the Rylington Merino flock plus a further 13 unrelated parental animals from a three generation half sibling sheep pedigree. The availability of an independently confirmed pedigree constructed from a three generation half sibling sheep family permitted the identification by deduction of central region MHC haplotypes based on a panel of SNPs derived from 10 loci. This is the first reporting of haplotypes covering this region of the sheep MHC. Analysis of SNP panel genotypes in the cohort of 71 unrelated sheep using the expectation maximization algorithm permitted the prediction of a group of approximately 20 haplotypes, which accounted for more than 90% of the expected haplotype distribution. Four of these predicted haplotypes were also present in the known haplotype cohort deduced from the sheep pedigree. Analysis of pairwise linkage disequilibrium between SNP loci in the cohort of 71 unrelated sheep showed a centre-most region displaying relatively high levels of linkage disequilibrium which was bounded by two regions displaying more variable linkage disequilibrium.It is hypothesised that this mid region of the central region of the sheep MHC may be a block like structure characterized by low recombination similar to those that have been widely described in the human and mouse genomes. The discoveries reported in this thesis provide a more accurate and detailed description of the central region of the sheep MHC together with a panel of SNPs, which reflect the diversity of this important genomic region which is known to be associated with immune responsiveness. The description, for the first time, of central region haplotypes provides a practical means of seeking candidate loci associated with disease resistance and productivity traits. The application of molecular techniques will enhance the rate at which the genomic composition of this region is elucidated and the work described in this thesis will contribute to final characterization of this important complex in health and disease.
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4

Feichtlbauer-Huber, Petra. "Einfluss des major histocompatibility complex (MHC) auf die Nematodenanfälligkeit beim Schaf." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964457458.

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5

Miltiadou, Despoin. "Characterization of the ovine Major Histocompatibility Complex (MHC) class I genes." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29891.

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To develop cellular and molecular tools to support development of vaccines against intracellular pathogens of sheep, a molecular genetic analysis of four distinct ovine MHC haplotypes carried by two heterozygous Blackface rams (501 and 504) was conducted. A total of 17 novel sequences was identified, 11 of which were obtained full length. Phylogenetic analysis using the identified transcripts and published ovine, bovine and other ruminant class I sequences belonging to the Bovidae family indicated that there are at least six ovine MHC class I loci (chapter 6). Sequence N1 and N2 are closer to the non classical bovine MHC class I sequence HD15 than to the remaining ovine class I transcripts. Seven out of eight full length transcripts subcloned into a mammalian expression vector expressed detectable class I cell surface glycoproteins in COS-7 cells (chapter 7). The combination of phylogenetic analysis, haplotype, transcription and expression data suggest that there are at least four distinct polymorphic ovine MHC class I loci, three of which appear to be expressed in a number of combinations in individual haplotypes, a couple of non polymorphic poorly transcribed class I like sequences and at least one additional diverged non classical class I locus (chapter 8). Similarities and differences of the ovine MHC class I region with that of other species and implications in immune response and sustainable control of intracellular sheep pathogens are discussed. Using the data generated here, an MHC defined sheep flock, which includes animals homozygous for each of the four MHC haplotypes, is currently under development. The MHC defined resource population, along with the transfected cell lines expressing each of the full length ovine MHC class I sequences, comprise tools for immunization and disease association experiments studying the protective immunity to intracellular pathogens of sheep.
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6

Lim, Elaine Hsuen. "Study of Fugu orthologues of mammalian MHC class III genes." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266288.

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7

Lo, Yun-hua. "A preliminary survey of MHC class I sequences in mandrills." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648208.

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8

Qin, Jinyi. "Characterisation of the central region of the sheep major histocompatibility complex." Curtin University of Technology, School of Biomedical Sciences, 2008. http://espace.library.curtin.edu.au:80/R/?func=dbin-jump-full&object_id=118317.

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The major histocompatibility complex (MHC) is a chromosomal region encoding molecules controlling adaptive immune response in vertebrates. In farm animals, many associations between MHC loci and productivity traits including disease susceptibility have been described. However, current knowledge about the structure and function of the MHC in domestic animals, especially sheep, is very limited. Characterization of the sheep MHC may potentially facilitate breeding for enhanced disease-resistant animals through use of marker assisted selection. The main aim of this project has been to provide insights into the organization of the genomic content of the central region of the sheep MHC. The work described herein has utilized subcloning of a sheep BAC genomic library in conjunction with DNA sequencing to generate a map of the central region of the sheep MHC covering ≈700 kbp. Within this map the relative order and identity of twenty five recognized loci were established. For some loci the intergenic distances were also determined. The final map is the most accurate map of this region reported to date and shows a high degree of similarity to the analogous region of the human MHC. This work has been published and a copy of the paper is included in Appendix 1. During the course of this work detailed genomic sequences were obtained for several sheep central region loci. Complete nucleotide sequences were generated for the complement factor B locus (CFB) and the TNFα locus and a comparative analysis of these sequences confirmed their homology with other vertebrate orthologues. Extensive partial sequences for complement components C2 and C4 were also obtained and reported to GenBank.
In addition, a previously identified short tandem repeat locus designated BfMs believed to be in the CFB locus was mapped to an intron within the adjacent SKI2VL locus. Single nucleotide polymorphisms (SNPs) were identified by analysing homologous sequences from a minimum of five individual sheep. In total 33 SNPs were discovered distributed over eleven distinct loci. Allele frequencies for SNPs from ten of these loci were determined and reported for a panel of 71 sheep comprising 58 unrelated sheep from the Rylington Merino flock plus a further 13 unrelated parental animals from a three generation half sibling sheep pedigree. The availability of an independently confirmed pedigree constructed from a three generation half sibling sheep family permitted the identification by deduction of central region MHC haplotypes based on a panel of SNPs derived from 10 loci. This is the first reporting of haplotypes covering this region of the sheep MHC. Analysis of SNP panel genotypes in the cohort of 71 unrelated sheep using the expectation maximization algorithm permitted the prediction of a group of approximately 20 haplotypes, which accounted for more than 90% of the expected haplotype distribution. Four of these predicted haplotypes were also present in the known haplotype cohort deduced from the sheep pedigree. Analysis of pairwise linkage disequilibrium between SNP loci in the cohort of 71 unrelated sheep showed a centre-most region displaying relatively high levels of linkage disequilibrium which was bounded by two regions displaying more variable linkage disequilibrium.
It is hypothesised that this mid region of the central region of the sheep MHC may be a block like structure characterized by low recombination similar to those that have been widely described in the human and mouse genomes. The discoveries reported in this thesis provide a more accurate and detailed description of the central region of the sheep MHC together with a panel of SNPs, which reflect the diversity of this important genomic region which is known to be associated with immune responsiveness. The description, for the first time, of central region haplotypes provides a practical means of seeking candidate loci associated with disease resistance and productivity traits. The application of molecular techniques will enhance the rate at which the genomic composition of this region is elucidated and the work described in this thesis will contribute to final characterization of this important complex in health and disease.
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9

Parker, Kay Elizabeth. "Genetic and immunological studies on class I MHC antigens of the rat." Thesis, Open University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.278511.

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10

Rogers, Sarah Louise. "Characterisation of C-type lectin-like receptor genes in the chicken MHC." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271871.

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Books on the topic "Major histocompatibility complex I (MHCI)"

1

Rammensee, Hans-Georg. MHC ligands and peptide motifs. Austin, Tex: Landes Bioscience, 1997.

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2

1956-, Srivastava Rakesh, Ram Bhanu P. 1951-, and Tyle Praveen 1960-, eds. Immunogenetics of the major histocompatibility complex. New York, N.Y: VCH, 1991.

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Natural history of the major histocompatibility complex. New York: Wiley, 1986.

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Harding, Clifford V. MHC molecules and antigen processing. Austin, Tex: R.G. Landes Co., 1997.

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H, Powis Stephen, and Vaughan Robert W, eds. MHC protocols. Totowa, N.J: Humana Press, 2003.

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1943-, Peña José, ed. MHC antigens and NK cells. Austin: R.G. Landes, 1994.

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Dr, Fernandez Nelson, and Butcher G, eds. MHC: A practical approach. Oxford: Oxford University Press, 1997.

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Michael, Browning, and McMichael Andrew J, eds. HLA and MHC: Genes, molecules and function. Oxford: BIOS Scientific, 1996.

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Kasahara, Masanori, ed. Major Histocompatibility Complex. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9.

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Klein, Jan. Natural history of the major histocompatibility complex. New York: Wiley, 1986.

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Book chapters on the topic "Major histocompatibility complex I (MHCI)"

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Tanaka, Keiji, Nobuyuki Tanahashi, and Naoki Shimbara. "Proteasomes and MHC class I-peptide generation." In Major Histocompatibility Complex, 203–12. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_14.

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Bauer, Dagmar, Frank Momburg, and Hartmut Hengel. "Manipulation of MHC-encoded proteins by cytomegaloviruses." In Major Histocompatibility Complex, 305–19. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_23.

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Naruse, Kiyoshi, Akihiro Shima, and Masaru Nonaka. "MHC gene organization of the bony fish, medaka." In Major Histocompatibility Complex, 91–109. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_7.

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Ellis, Shirley A., Edward C. Holmes, Karen A. Staines, and W. Ivan Morrison. "The evolution of MHC class I genes in cattle." In Major Histocompatibility Complex, 273–78. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_20.

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Böhme, Jan, and Kari Högstrand. "Sequence conditions for gene conversion of mouse MHC genes." In Major Histocompatibility Complex, 503–17. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_37.

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Godwin, Ulla B., Michael Flores, Thomas J. McConnell, Melanie R. Wilson, Sylvie Quiniou, Norman W. Miller, and L. William Clem. "Two MHC class II A loci in the channel catfish." In Major Histocompatibility Complex, 260–72. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_19.

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Kasahara, Masanori, Makoto Yawata, and Takashi Suzuki. "The MHC paralogous group: listing of members and a brief overview." In Major Histocompatibility Complex, 27–44. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_2.

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Udaka, Keiko, Karl-Heinz Wiesmüller, and Günther Jung. "Repertoire forecast of MHC class I binding peptides with peptide libraries." In Major Histocompatibility Complex, 487–502. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_36.

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Du Pasquier, Louis. "Relationships among the genes encoding MHC molecules and the specific antigen receptors." In Major Histocompatibility Complex, 53–65. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_4.

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Morales, Pablo, Jorge Martinez-Laso, Maria Jose Castro, Eduardo Gomez-Casado, Miguel Alvarez, Ricardo Rojo, Javier Longas, Ernesto Lowy, Isabel Rubio, and Antonio Arnaiz-Villena. "An evolutionary overview of the MHC-G polymorphism: clues to the unknown function(s)." In Major Histocompatibility Complex, 463–79. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-65868-9_34.

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Conference papers on the topic "Major histocompatibility complex I (MHCI)"

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Knoche, Shelby M., Gabrielle L. Brumfield, Benjamin T. Goetz, Bailee H. Sliker, Cecilia Barbosa, Svetlana Romanova, Tatiana Bronich, Donald W. Coulter, and Joyce C. Solheim. "Abstract P028: Effects of histone deacetylase inhibition on major histocompatibility compatibility complex (MHC) class I expression, growth, and migration of cancer cells." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-p028.

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Qiu, Xuemei, Feng Zhang, Xiangying Meng, Yibing Zhou, and Xiuli Wang. "Evolution of the Major Histocompatibility Complex Genes in Fish." In 2009 3rd International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2009. http://dx.doi.org/10.1109/icbbe.2009.5162809.

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Rowland, A., G. Levine, L. Schnabel, A. Berglund, D. Antczak, D. Miller, and Watts AE. "Allorecognition of Mesenchymal Stem Cells is Dependent on Major Histocompatibility Complex Haplotype." In Abstracts of the 47th Annual Conference of the Veterinary Orthopedic Society. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1712896.

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Sroka, Ewa Maria, Rodrigo Prado Martins, Chrysoula Daskalogianni, Sebastien Apcher, and Robin Fahraeus. "Abstract B187: Origins of neoantigens for the major histocompatibility complex class I pathway." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b187.

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Ford, Michael, Richard Jones, David Allen, Ravi Amunugama, Paul Del Rizzo, Michael Pisano, James Mobley, et al. "Abstract B80: Mass spectrometric characterization of peptides associated with molecules of the major histocompatibility complex." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b80.

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Ford, Michael, Richard Jones, David Allen, Ravi Amunugama, Paul Del Rizzo, Michael Pisano, James Mobley, Paul Domanski, Bill Ho, and Daniel Bochar. "Abstract 1673: Mass spectrometric characterization of peptides associated with molecules of the major histocompatibility complex." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1673.

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Knoche, Shelby M., and Joyce C. Solheim. "Abstract 1817: Epidermal growth factor receptor alters major histocompatibility complex class I expression on pancreatic cancer cells." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1817.

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Bustos, MA, JIJ Orozco, MP Salomon, DSB Hoon, and DM Marzese. "Abstract P1-05-02: CRISPR/Cas9-guided editing of spliceosome factors enhances major histocompatibility complex proteins in triple-negative breast cancer." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p1-05-02.

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Klimanov, Igor A., Svetlana Soodaeva, Timur Li, Nailya Kubysheva, Larisa Postnikova, Viktor Novikov, and Lidiya Nikitina. "Level of soluble molecules of major histocompatibility complex CLASS II in serum, sputum and exhaled breath condensate in COPD of patients with an exacerbation of COPD." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa885.

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Reports on the topic "Major histocompatibility complex I (MHCI)"

1

Lamont, Susan J., E. Dan Heller, and Avigdor Cahaner. Prediction of Immunocompetence and Resistance to Disease by Using Molecular Markers of the Major Histocompatibility Complex. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7568780.bard.

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Abstract:
This project utilized two live-animal populations in an integrated research program to identify molecular markers for immune response and disease resistance. The populations each had their foundation from meat-type commercial breeder chicken lines of their respective countries. Investigations effectively used unique availability of resources in each country to study commercial-type environments in Israel and line-crosses with diverse inbred lines in the US. Two bacterial systems were investigated to cover both respiratory and gastrointestinal, and primary and secondary, infections. Individual experimental groups of animals were evaluated for combinations of vaccine antibody levels, response to pathogen challenge, growth parameters, genetic background and molecular markers. The positive association of antibody level with resistance to disease was confirmed. Effectiveness of genetic selection for vaccine antibody response level was demonstrated. Molecular markers, both inside and outside the MHC region, were associated with antibody response and resistance to disease. Markers were shown to have a generalized effect, by association with multiple traits of immune response and disease resistance. The impact of genetic background on marker effect was shown to be important. The overall results demonstrate the effectiveness of selection on vaccine antibody response and the potential of molecular marker-assisted selection to improve efficiency of production of meat-type chickens by reducing genetic susceptibility to disease.
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