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Journal articles on the topic 'Signalling protein MHC Class I'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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1

Slade, J. W. G., M. J. Watson, T. R. Kelly, G. B. Gloor, M. A. Bernards, and E. A. MacDougall-Shackleton. "Chemical composition of preen wax reflects major histocompatibility complex similarity in songbirds." Proceedings of the Royal Society B: Biological Sciences 283, no. 1842 (2016): 20161966. http://dx.doi.org/10.1098/rspb.2016.1966.

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In jawed vertebrates, genes of the major histocompatibility complex (MHC) play a key role in immunity by encoding cell-surface proteins that recognize and bind non-self antigens. High variability at MHC suggests that these loci may also function in social signalling such as mate choice and kin recognition. This requires that MHC genotype covaries with some perceptible phenotypic trait. In mammals and fish, MHC is signalled chemically through volatile and non-volatile peptide odour cues, facilitating MHC-dependent mate choice and other behaviours. In birds, despite evidence for MHC-dependent ma

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2

Ellwanger, Kornelia, Christine Kienzle, Sylke Lutz, et al. "Protein kinase D controls voluntary-running-induced skeletal muscle remodelling." Biochemical Journal 440, no. 3 (2011): 327–35. http://dx.doi.org/10.1042/bj20101980.

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Skeletal muscle responds to exercise by activation of signalling pathways that co-ordinate gene expression to sustain muscle performance. MEF2 (myocyte enhancer factor 2)-dependent transcriptional activation of MHC (myosin heavy chain) genes promotes the transformation from fast-twitch into slow-twitch fibres, with MEF2 activity being tightly regulated by interaction with class IIa HDACs (histone deacetylases). PKD (protein kinase D) is known to directly phosphorylate skeletal muscle class IIa HDACs, mediating their nuclear export and thus derepression of MEF2. In the present study, we report

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3

Krummel, Matthew, Christoph Wülfing, Cenk Sumen, and Mark M. Davis. "Thirty–six views of T–cell recognition." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1400 (2000): 1071–76. http://dx.doi.org/10.1098/rstb.2000.0644.

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While much is known about the signalling pathways within lymphocytes that are triggered during activation, much less is known about how the various cell surface molecules on T cells initiate these events. To address this, we have focused on the primary interaction that drives T–cell activation, namely the binding of a particular T–cell receptor (TCR) to peptide–MHC ligands, and find a close correlation between biological activity and off–rate; that is, the most stimulatory TCR ligands have the slowest dissociation rates. In general, TCRs from multiple histocompatibility complex (MHC) class–II–

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4

SINGH, MANISH K., FAUZIA JAMAL, AMIT K. DUBEY, et al. "Co-factor-independent phosphoglycerate mutase of Leishmania donovani modulates macrophage signalling and promotes T-cell repertoires bearing epitopes for both MHC-I and MHC-II." Parasitology 145, no. 3 (2017): 292–306. http://dx.doi.org/10.1017/s0031182017001494.

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SUMMARYImmunoactivation depends upon the antigen potential to modulate T-cell repertoires. The present study has enumerated the effect of 61 kDa recombinant Leishmania donovani co-factor-independent phosphoglycerate mutase (rLd-iPGAM) on mononuclear cells of healthy and treated visceral leishmaniasis subjects as well as on THP-1 cell line. rLd-iPGAM stimulation induced higher expression of interleukin-1β (IL-1β) in the phagocytic cell, its receptor and CD69 on T-cell subsets. These cellular activations resulted in upregulation of host-protective cytokines IL-2, IL-12, IL-17, tumour necrosis fa

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Athanassakis, Irene. "Analysis of the IFN-γ-induced signal transduction pathway in fetal rejection". Mediators of Inflammation 4, № 3 (1995): 209–16. http://dx.doi.org/10.1155/s0962935195000342.

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The placenta, one of the most important fetal tissues during gestation, ensures nutrition, development and protection of the fetus. Although placenta lacks expression of class II MHC antigens, they can be induced either by interferon-gamma (IFN-γ) on the spongiotrophoblast zone, or by 5-azacytidine (5-azaC) on the labyrinthine trophoblast zone, two agents actively participating in a plethora of immunological and inflammatory reactions. This induction is correlated with fetal abortion and fetal developmental abnormalities. In this work thein vitroandin vivosignal transduction pathways followed

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6

Fairley, J. A., J. Baillie, M. Bain, and J. H. Sinclair. "Human cytomegalovirus infection inhibits epidermal growth factor (EGF) signalling by targeting EGF receptors." Journal of General Virology 83, no. 11 (2002): 2803–10. http://dx.doi.org/10.1099/0022-1317-83-11-2803.

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Infection with human cytomegalovirus (HCMV) is known to involve complex interactions between viral and cellular factors resulting in perturbation of a number of cellular functions. Specifically, HCMV infection targets control of the cell cycle, cellular transcription and immunoregulation, presumably to optimize the cellular environment for virus persistence and productive infection. Here, we show that HCMV infection also prevents external signalling to the cell by disrupting the function of epidermal growth factor receptor (EGFR). Infection with HCMV resulted in a decrease in cell-surface expr

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7

Vassiliadis, S., N. Kyrpides, D. Stravopodis, M. Grigoriou, I. Athanassakis та J. Papamatheakis. "Investigation of intracellular signals generated by γ-interferon and IL-4 leading to the induction of class II antigen expression". Mediators of Inflammation 2, № 5 (1993): 343–48. http://dx.doi.org/10.1155/s096293519300047x.

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Signal transduction plays a vital role in cellular behaviour as cells respond to various stimuli in different ways and utilize diverse pathways for accomplishing their task. Determination of the pathway followed by various cytokines can be achieved using specific inhibitors which include theophylline (TPH), TMB-8 and W7 that hinder calmodulin binding to Ca2+; sphingosine (SPH), H7 and staurosporine that inhibit protein kinase C (PKC) activation; and mevalonate (MEV) or the anti-p21rasantibody which block G-proteins. This study shows that the immunologically important class II antigens in human

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8

Tan, H., J. A. West, J. P. Ramsay, et al. "Comprehensive overexpression analysis of cyclic-di-GMP signalling proteins in the phytopathogen Pectobacterium atrosepticum reveals diverse effects on motility and virulence phenotypes." Microbiology 160, no. 7 (2014): 1427–39. http://dx.doi.org/10.1099/mic.0.076828-0.

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Bis-(3′-5′)-cyclic dimeric guanosine monophosphate (c-di-GMP) is a ubiquitous bacterial signalling molecule produced by diguanylate cyclases of the GGDEF-domain family. Elevated c-di-GMP levels or increased GGDEF protein expression is frequently associated with the onset of sessility and biofilm formation in numerous bacterial species. Conversely, phosphodiesterase-dependent diminution of c-di-GMP levels by EAL- and HD-GYP-domain proteins is often accompanied by increased motility and virulence. In this study, we individually overexpressed 23 predicted GGDEF, EAL or HD-GYP-domain proteins enco

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van Loenen, Marleen M., Renate S. Hagedoorn, Roelof Willemze, J. H. Frederik Falkenburg та Mirjam H. M. Heemskerk. "Extracellular Domains of CD8a and β Subunits Are Required and Sufficient for HLA Class I Restricted Helper Activity of TCR-Engineered CD4+ T Cells." Blood 114, № 22 (2009): 3574. http://dx.doi.org/10.1182/blood.v114.22.3574.3574.

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Abstract Abstract 3574 Poster Board III-511 Adoptive transfer of T cell receptor (TCR)-transferred T cells may be an attractive strategy to treat patients with hematological malignancies relapsing after allogeneic stem cell transplantation. Transfer of HLA class I restricted TCRs into CD8+ T cells demonstrated redirected antigen specificity. However, for persistence of anti-leukemic responses in vivo, CD4+ T cells may be important. Therefore, redirecting specificity of CD4+ T cells with well defined HLA class I restricted TCRs might be an attractive strategy for providing help. HLA class I res

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Lacey, Melissa M., Jonathan D. Partridge, and Jeffrey Green. "Escherichia coli K-12 YfgF is an anaerobic cyclic di-GMP phosphodiesterase with roles in cell surface remodelling and the oxidative stress response." Microbiology 156, no. 9 (2010): 2873–86. http://dx.doi.org/10.1099/mic.0.037887-0.

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The Escherichia coli K-12 yfgF gene encodes a protein with domains associated with cyclic di-GMP signalling: GGDEF (associated with diguanylate cyclase activity) and EAL (associated with cyclic di-GMP phosphodiesterase activity). Here, it is shown that yfgF is expressed under anaerobic conditions from a class II FNR (regulator of fumarate and nitrate reduction)-dependent promoter. Anaerobic expression of yfgF is greatest in stationary phase, and in cultures grown at 28 °C, suggesting that low growth rates promote yfgF expression. Mutation of yfgF resulted in altered cell surface properties and

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11

Koivula, Satu, Minna Taskinen, Ping Chen, et al. "Exon-Based Transcriptome Profiling Reveals Genes That Have Prognostic Impact on the Survival of Young High Risk Diffuse Large B-Cell/Follicular Grade 3 Lymphoma Patients Treated with Dose-Dense Chemoimmunotherapy and CNS Prophylaxis. Results From a Nordic Lymphoma Group Phase II Study." Blood 116, no. 21 (2010): 3107. http://dx.doi.org/10.1182/blood.v116.21.3107.3107.

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Abstract Abstract 3107 Background: Survival of young high risk diffuse large B-cell lymphoma (DLBCL) is now approaching 80% due to implementation of rituximab and dose-dense chemotherapy protocols but the patients with relapsed or refractory disease continue to have a poor prognosis. Such patients could benefit from additional therapies if their clinical outcome could be more accurately predicted at the time of diagnosis. Recently, several gene-expression signatures with prognostic significance in DLBCL have been identified. To date, the accessibility of exon arrays that interrogate exon-level

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Aguilar, Maria Montserrat, Matthew D. Blunt, Jonathan C. Strefford, et al. "IL-4 Exerts Opposing Effects on Surface-IgM and CXCR4 Mediated Signalling in Chronic Lymphocytic Leukaemia." Blood 124, no. 21 (2014): 3299. http://dx.doi.org/10.1182/blood.v124.21.3299.3299.

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Abstract The B cell receptor (BCR) is critical for survival and proliferation of chronic lymphocytic leukemia (CLL) cells and is activated following antigen/autoantigen engagement. BCR engagement in vivo triggers a partial receptor down modulation, phosphorylation of tyrosine residues in CD79A and CD79B, signalosome formation and subsequent calcium mobilization and ERK phosphorylation (ERK-P). Interestingly CLL cells incubated in vitro recover surface(s)IgM receptor expression and subsequently their ability to signal (calcium flux and ERK-P). During this recovery of sIgM, expression of a fully

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Vassiliadis, Simon. "Analysis of Signals Leading to Differentiation of Immature HL-60 after Administration of IL-4." Mediators of Inflammation 3, no. 6 (1994): 415–18. http://dx.doi.org/10.1155/s096293519400058x.

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Treatment of acute myeloid leukaemia (AML) cells with differentiation agents leads not only to the acquisition of normal phenotypes but also contributes to the understanding of special immuno-haematology issues. For instance, induction of HLA-DR antigens on human promyelocytic leukaemia HL-60 cells by interleukin-4 (IL-4) is of pivotal importance in immunology not only because class II expression is prerequisite to antigen recognition and response but also because IL-4 participates in a plethora of inflammatory or non-inflammatory reactions. At the same time, the same observation coupled with

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14

Bird, Lucy. "MHC class I as a negative regulator of TLR signalling." Nature Reviews Immunology 12, no. 6 (2012): 401. http://dx.doi.org/10.1038/nri3243.

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15

Adamski, Jill, Zhendong Ma, Susan Nozell та Etty N. Benveniste. "17β-Estradiol Inhibits Class II Major Histocompatibility Complex (MHC) Expression: Influence on Histone Modifications and CBP Recruitment to the Class II MHC Promoter". Molecular Endocrinology 18, № 8 (2004): 1963–74. http://dx.doi.org/10.1210/me.2004-0098.

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Abstract Major histocompatibility complex (MHC) class II proteins are important for the initiation of immune responses and are essential for specific recognition of foreign antigens by the immune system. Regulation of class II MHC expression primarily occurs at the transcriptional level. The class II transactivator protein is the master regulator that is essential for both constitutive and interferon-γ-inducible class II MHC expression. Estrogen [17β-estradiol (17β-E2)] has been shown to have immunomodulatory effects. In this study, we show that 17β-E2 down-regulates interferon-γ inducible cla

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Fortier, Marie-Hélène, Etienne Caron, Danielle De Verteuil, Claude Perreault, and Pierre Thibault. "Influence of mTOR Signalling Pathway on the MHC I Immunopeptidome." Blood 110, no. 11 (2007): 3887. http://dx.doi.org/10.1182/blood.v110.11.3887.3887.

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Abstract Cell surface major histocompatibility complex (MHC) I molecules are associated with self peptides that are collectively referred to as the self MHC I immunopeptidome (sMII). Despite the tremendous importance of the sMII, very little is known on its genesis and molecular composition. On the other hand, it is well established that the signalling pathway involving mammalian target of rapamycin (mTOR) plays an essential role in the regulation of processes such as ribosome biogenesis and protein translation which are critical for cell growth, proliferation and differentiation. In this work

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FROSCH, S., U. BONIFAS, R. ROß, et al. "Costimulatory signalling potential of murine MHC class II‐positive T‐clone cells." Immunology 89, no. 3 (1996): 384–90. http://dx.doi.org/10.1046/j.1365-2567.1996.d01-748.x.

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18

Abendroth, Allison, Barry Slobedman, Eunice Lee, Elizabeth Mellins, Mark Wallace, and Ann M. Arvin. "Modulation of Major Histocompatibility Class II Protein Expression by Varicella-Zoster Virus." Journal of Virology 74, no. 4 (2000): 1900–1907. http://dx.doi.org/10.1128/jvi.74.4.1900-1907.2000.

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ABSTRACT We sought to investigate the effects of varicella-zoster virus (VZV) infection on gamma interferon (IFN-γ)-stimulated expression of cell surface major histocompatibility complex (MHC) class II molecules on human fibroblasts. IFN-γ treatment induced cell surface MHC class II expression on 60 to 86% of uninfected cells, compared to 20 to 30% of cells which had been infected with VZV prior to the addition of IFN-γ. In contrast, cells that were treated with IFN-γ before VZV infection had profiles of MHC class II expression similar to those of uninfected cell populations. Neither IFN-γ tre

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19

Trgovcich, Joanne, Colleen Cebulla, Pete Zimmerman, and Daniel D. Sedmak. "Human Cytomegalovirus Protein pp71 Disrupts Major Histocompatibility Complex Class I Cell Surface Expression." Journal of Virology 80, no. 2 (2006): 951–63. http://dx.doi.org/10.1128/jvi.80.2.951-963.2006.

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ABSTRACT The human cytomegalovirus tegument protein pp71 is the product of the UL82 gene. Roles for pp71 in stimulating gene transcription, increasing infectivity of viral DNA, and the degradation of retinoblastoma family proteins have been described. Here we report a novel function for pp71 in limiting accumulation of cell surface major histocompatibility complex (MHC) class I complexes. MHC molecules were analyzed in glioblastoma cells exposed to a replication-defective adenovirus expressing UL82 (Adpp71) or after transient transfection of the UL82 gene. Accumulation of cell surface MHC clas

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Masaki, Kento, Yuhji Hiraki, Hiroka Onishi, et al. "Ligation of MHC Class II Induces PKC-Dependent Clathrin-Mediated Endocytosis of MHC Class II." Cells 9, no. 8 (2020): 1810. http://dx.doi.org/10.3390/cells9081810.

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In addition to antigen presentation to CD4+ T cells, aggregation of cell surface major histocompatibility complex class II (MHC-II) molecules induces signal transduction in antigen presenting cells that regulate cellular functions. We previously reported that crosslinking of MHC-II induced the endocytosis of MHC-II, which was associated with decreased surface expression levels in murine dendritic cells (DCs) and resulted in impaired activation of CD4+ T cells. However, the downstream signal that induces MHC-II endocytosis remains to be elucidated. In this study, we found that the crosslinking

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Setterblad, N., S. Becart, D. Charron, and N. Mooney. "Signalling via MHC Class II Molecules Modifies the Composition of GEMs in APC." Scandinavian Journal of Immunology 54, no. 1-2 (2001): 87–92. http://dx.doi.org/10.1046/j.1365-3083.2001.00969.x.

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22

Cosman, David, Neil Fanger, and Luis Borges. "Human cytomegalovirus, MHC class I and inhibitory signalling receptors: more questions than answers." Immunological Reviews 168, no. 1 (1999): 177–85. http://dx.doi.org/10.1111/j.1600-065x.1999.tb01292.x.

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Hirano, Junki, Sachiyo Yoshio, Yusuke Sakai, et al. "Hepatitis C virus modulates signal peptide peptidase to alter host protein processing." Proceedings of the National Academy of Sciences 118, no. 22 (2021): e2026184118. http://dx.doi.org/10.1073/pnas.2026184118.

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Immunoevasins are viral proteins that prevent antigen presentation on major histocompatibility complex (MHC) class I, thus evading host immune recognition. Hepatitis C virus (HCV) evades immune surveillance to induce chronic infection; however, how HCV-infected hepatocytes affect immune cells and evade immune recognition remains unclear. Herein, we demonstrate that HCV core protein functions as an immunoevasin. Its expression interfered with the maturation of MHC class I molecules catalyzed by the signal peptide peptidase (SPP) and induced their degradation via HMG-CoA reductase degradation 1

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Tardif, Keith D., and Aleem Siddiqui. "Cell Surface Expression of Major Histocompatibility Complex Class I Molecules Is Reduced in Hepatitis C Virus Subgenomic Replicon-Expressing Cells." Journal of Virology 77, no. 21 (2003): 11644–50. http://dx.doi.org/10.1128/jvi.77.21.11644-11650.2003.

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ABSTRACT The hepatitis C virus (HCV) causes chronic hepatitis in most infected individuals by evading host immune defenses. In this investigation, we show that HCV-infected cells may go undetected in the immune system by suppressing major histocompatibility complex (MHC) class I antigen presentation to cytotoxic T lymphocytes. Cells expressing HCV subgenomic replicons have lower MHC class I cell surface expression. This is due to reduced levels of properly folded MHC class I molecules. HCV replicons induce endoplasmic reticulum (ER) stress (K. Tardif, K. Mori, and A. Siddiqui, J. Virol. 76:745

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Misaghi, Shahram, Zhen-Yu J. Sun, Patrick Stern, Rachelle Gaudet, Gerhard Wagner, and Hidde Ploegh. "Structural and Functional Analysis of Human Cytomegalovirus US3 Protein." Journal of Virology 78, no. 1 (2004): 413–23. http://dx.doi.org/10.1128/jvi.78.1.413-423.2004.

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ABSTRACT Human cytomegalovirus (HCMV) unique short region 3 (US3) protein, a type I membrane protein, prevents maturation of class I major histocompatibility complex (MHC) molecules by retaining them in the endoplasmic reticulum (ER) and thus helps inhibit antigen presentation to cytotoxic T cells. US3 molecules bind to class I MHC molecules in a transient fashion but retain them very efficiently in the ER nonetheless. The US3 luminal domain is responsible for ER retention of US3 itself, while both the US3 luminal and transmembrane domains are necessary for retaining class I MHC in the ER. We

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Koppers-Lalic, Danijela, Frans A. M. Rijsewijk, Sylvia B. E. Verschuren, et al. "The UL41-encoded virion host shutoff (vhs) protein and vhs-independent mechanisms are responsible for down-regulation of MHC class I molecules by bovine herpesvirus 1." Journal of General Virology 82, no. 9 (2001): 2071–81. http://dx.doi.org/10.1099/0022-1317-82-9-2071.

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The virion host shutoff (vhs) protein of alphaherpesviruses causes a rapid shutoff of host cell protein synthesis. We constructed a bovine herpesvirus 1 (BHV1) deletion mutant in which the putative vhs gene, UL41, has been disrupted. Whereas protein synthesis is inhibited within 3 h after infection with wild-type BHV1, no inhibition was observed after infection with the BHV1vhs− deletion mutant. These results indicate that the BHV1 UL41 gene product is both necessary and sufficient for shutoff of host cell protein synthesis at early times post-infection. Using the vhs deletion mutant, we inves

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Kinch, M. S., A. Sanfridson, and C. Doyle. "The protein tyrosine kinase p56lck regulates cell adhesion mediated by CD4 and major histocompatibility complex class II proteins." Journal of Experimental Medicine 180, no. 5 (1994): 1729–39. http://dx.doi.org/10.1084/jem.180.5.1729.

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The CD4 protein is expressed on a subset of human T lymphocytes that recognize antigen in the context of major histocompatibility complex (MHC) class II molecules. Using Chinese hamster ovary (CHO) cells expressing human CD4, we have previously demonstrated that the CD4 protein can mediate cell adhesion by direct interaction with MHC class II molecules. In T lymphocytes, CD4 can also function as a signaling molecule, presumably through its intracellular association with p56lck, a member of the src family of protein tyrosine kinases. In the present report, we show that p56lck can affect cell ad

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Vascotto, Fulvia, Danielle Lankar, Gabrielle Faure-André, et al. "The actin-based motor protein myosin II regulates MHC class II trafficking and BCR-driven antigen presentation." Journal of Cell Biology 176, no. 7 (2007): 1007–19. http://dx.doi.org/10.1083/jcb.200611147.

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Antigen (Ag) capture and presentation onto major histocompatibility complex (MHC) class II molecules by B lymphocytes is mediated by their surface Ag receptor (B cell receptor [BCR]). Therefore, the transport of vesicles that carry MHC class II and BCR–Ag complexes must be coordinated for them to converge for processing. In this study, we identify the actin-associated motor protein myosin II as being essential for this process. Myosin II is activated upon BCR engagement and associates with MHC class II–invariant chain complexes. Myosin II inhibition or depletion compromises the convergence and

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Tomai, M., M. Kotb, G. Majumdar, and E. H. Beachey. "Superantigenicity of streptococcal M protein." Journal of Experimental Medicine 172, no. 1 (1990): 359–62. http://dx.doi.org/10.1084/jem.172.1.359.

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M proteins that define the serotypes of group A streptococci are powerful blastogens for human T lymphocytes. The mechanism by which they activate T cells was investigated and compared with the conventional T cell mitogen phytohemagglutinin, and the known superantigen staphylococcal enterotoxin B. Although major histocompatibility complex (MHC) class II molecules are required for presentation, there is no MHC restriction, since allogeneic class II molecules presented the bacterial protein to human T cells. Type 5 M protein appears to bind class II molecules on the antigen-presenting cells and

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Wang, Jinguo, and Tomasz I. Michalak. "Inhibition by Woodchuck Hepatitis Virus of Class I Major Histocompatibility Complex Presentation on Hepatocytes Is Mediated by Virus Envelope Pre-S2 Protein and Can Be Reversed by Treatment with Gamma Interferon." Journal of Virology 80, no. 17 (2006): 8541–53. http://dx.doi.org/10.1128/jvi.00830-06.

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ABSTRACT Presentation of class I major histocompatibility complex (MHC) is severely down-regulated on hepatocytes in chronic hepatitis caused by woodchuck hepatitis virus (WHV). To determine which of the viral proteins mediates class I MHC antigen suppression, cultured normal woodchuck hepatocytes were transfected with the complete WHV genome, sequences encoding individual virus proteins, or whole virus genomes in which transcription of selected proteins was disabled by site-specific mutagenesis. It was found that hepatocyte presentation of class I MHC antigen was significantly inhibited follo

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Zang, Weiping, Safa Kalache, Marvin Lin, Bernd Schroppel, and Barbara Murphy. "MHC Class II–Mediated Apoptosis by a Nonpolymorphic MHC Class II Peptide Proceeds by Activation of Protein Kinase C." Journal of the American Society of Nephrology 16, no. 12 (2005): 3661–68. http://dx.doi.org/10.1681/asn.2005050523.

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Frauman, A. G., P. Chu, and L. C. Harrison. "Nonimmune thyroid destruction results from transgenic overexpression of an allogeneic major histocompatibility complex class I protein." Molecular and Cellular Biology 13, no. 3 (1993): 1554–64. http://dx.doi.org/10.1128/mcb.13.3.1554.

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The overexpression of major histocompatibility complex (MHC) class I molecules in endocrine epithelial cells is an early feature of autoimmune thyroid disease and insulin-dependent diabetes mellitus, which may reflect a cellular response, e.g., to viruses or toxins. Evidence from a transgenic model in pancreatic beta cells suggests that MHC class I overexpression could play an independent role in endocrine cell destruction. We demonstrate in this study that the transgenic overexpression of an allogeneic MHC class I protein (H-2Kb) linked to the rat thyroglobulin promoter, in H-2Kk mice homozyg

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Frauman, A. G., P. Chu, and L. C. Harrison. "Nonimmune thyroid destruction results from transgenic overexpression of an allogeneic major histocompatibility complex class I protein." Molecular and Cellular Biology 13, no. 3 (1993): 1554–64. http://dx.doi.org/10.1128/mcb.13.3.1554-1564.1993.

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The overexpression of major histocompatibility complex (MHC) class I molecules in endocrine epithelial cells is an early feature of autoimmune thyroid disease and insulin-dependent diabetes mellitus, which may reflect a cellular response, e.g., to viruses or toxins. Evidence from a transgenic model in pancreatic beta cells suggests that MHC class I overexpression could play an independent role in endocrine cell destruction. We demonstrate in this study that the transgenic overexpression of an allogeneic MHC class I protein (H-2Kb) linked to the rat thyroglobulin promoter, in H-2Kk mice homozyg

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Guerreiro-Cacais, Andre Ortlieb, Mehmet Uzunel, Jelena Levitskaya та Victor Levitsky. "Inhibition of Heavy Chain and β2-Microglobulin Synthesis as a Mechanism of Major Histocompatibility Complex Class I Downregulation during Epstein-Barr Virus Replication". Journal of Virology 81, № 3 (2006): 1390–400. http://dx.doi.org/10.1128/jvi.01999-06.

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ABSTRACT The mechanisms of major histocompatibility complex (MHC) class I downregulation during Epstein-Barr virus (EBV) replication are not well characterized. Here we show that in several cell lines infected with a recombinant EBV strain encoding green fluorescent protein (GFP), the virus lytic cycle coincides with GFP expression, which thus can be used as a marker of virus replication. EBV replication resulted in downregulation of MHC class II and all classical MHC class I alleles independently of viral DNA synthesis or late gene expression. Although assembled MHC class I complexes, the tot

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Chang, C. H., J. D. Fontes, M. Peterlin, and R. A. Flavell. "Class II transactivator (CIITA) is sufficient for the inducible expression of major histocompatibility complex class II genes." Journal of Experimental Medicine 180, no. 4 (1994): 1367–74. http://dx.doi.org/10.1084/jem.180.4.1367.

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The class II transactivator (CIITA) has been shown to be required for major histocompatibility complex (MHC) class II gene expression in B cells and its deficiency is responsible for a hereditary MHC class II deficiency. Here we show that CIITA is also involved in the inducible expression of class II genes upon interferon gamma (IFN-gamma) treatment. The expression of CIITA is also inducible with IFN-gamma before the induction of MHC class II mRNA. In addition, CIITA mRNA expression does not require new protein synthesis, although new protein synthesis is necessary for the transcription of cla

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Inaba, Kayo, Shannon Turley, Tomonori Iyoda, et al. "The Formation of Immunogenic Major Histocompatibility Complex Class II–Peptide Ligands in Lysosomal Compartments of Dendritic Cells Is Regulated by Inflammatory Stimuli." Journal of Experimental Medicine 191, no. 6 (2000): 927–36. http://dx.doi.org/10.1084/jem.191.6.927.

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During their final differentiation or maturation, dendritic cells (DCs) redistribute their major histocompatibility complex (MHC) class II products from intracellular compartments to the plasma membrane. Using cells arrested in the immature state, we now find that DCs also regulate the initial intracellular formation of immunogenic MHC class II–peptide complexes. Immature DCs internalize the protein antigen, hen egg lysozyme (HEL), into late endosomes and lysosomes rich in MHC class II molecules. There, despite extensive colocalization of HEL protein and MHC class II products, MHC class II–pep

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Lu, H. T., J. L. Riley, G. T. Babcock, et al. "Interferon (IFN) beta acts downstream of IFN-gamma-induced class II transactivator messenger RNA accumulation to block major histocompatibility complex class II gene expression and requires the 48-kD DNA-binding protein, ISGF3-gamma." Journal of Experimental Medicine 182, no. 5 (1995): 1517–25. http://dx.doi.org/10.1084/jem.182.5.1517.

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Interferon (IFN) gamma, a cardinal proinflammatory cytokine, induces expression of the gene products of the class II locus of the major histocompatibility complex (MHC), whereas IFN-alpha or -beta suppresses MHC class II expression. The mechanism of IFN-beta-mediated MHC class II inhibition has been unclear. Recently, a novel factor termed class II transactivator (CIITA) has been identified as essential for IFN-gamma-induced MHC class II transcription. We studied the status of IFN-gamma-induced CIITA messenger RNA (mRNA) accumulation and CIITA-driven transactivation in IFN-beta-treated cells a

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Carbone, F. R., N. A. Hosken, M. W. Moore, and M. J. Bevan. "Class I MHC-restricted Cytotoxic Responses to Soluble Protein Antigen." Cold Spring Harbor Symposia on Quantitative Biology 54 (January 1, 1989): 551–55. http://dx.doi.org/10.1101/sqb.1989.054.01.065.

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Celie, Patrick H. N., Mireille Toebes, Boris Rodenko, Huib Ovaa, Anastassis Perrakis, and Ton N. M. Schumacher. "UV-Induced Ligand Exchange in MHC Class I Protein Crystals." Journal of the American Chemical Society 131, no. 34 (2009): 12298–304. http://dx.doi.org/10.1021/ja9037559.

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Marks, Michael S. "Protein sorting within the mhc class II antigen-processing pathway." Immunologic Research 17, no. 1-2 (1998): 141–54. http://dx.doi.org/10.1007/bf02786439.

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Casares, Sofia, Constantin A. Bona, and Teodor-D. Brumeanu. "Enzymatically mediated engineering of multivalent MHC class II–peptide chimeras." Protein Engineering, Design and Selection 14, no. 3 (2001): 195–200. http://dx.doi.org/10.1093/protein/14.3.195.

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Hake, Sandra B., Krzysztof Masternak, Claudia Kammerbauer, Christian Janzen, Walter Reith, and Viktor Steimle. "CIITA Leucine-Rich Repeats Control Nuclear Localization, In Vivo Recruitment to the Major Histocompatibility Complex (MHC) Class II Enhanceosome, and MHC Class II Gene Transactivation." Molecular and Cellular Biology 20, no. 20 (2000): 7716–25. http://dx.doi.org/10.1128/mcb.20.20.7716-7725.2000.

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ABSTRACT The major histocompatibility complex (MHC) class II transactivator CIITA plays a pivotal role in the control of the cellular immune response through the quantitative regulation of MHC class II expression. We have analyzed a region of CIITA with similarity to leucine-rich repeats (LRRs). CIITA LRR alanine mutations abolish both the transactivation capacity of full-length CIITA and the dominant-negative phenotype of CIITA mutants with N-terminal deletions. We demonstrate direct interaction of CIITA with the MHC class II promoter binding protein RFX5 and could also detect novel interacti

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Durand, B., M. Kobr, W. Reith, and B. Mach. "Functional complementation of major histocompatibility complex class II regulatory mutants by the purified X-box-binding protein RFX." Molecular and Cellular Biology 14, no. 10 (1994): 6839–47. http://dx.doi.org/10.1128/mcb.14.10.6839.

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Major histocompatibility complex (MHC) class II deficiency, or bare lymphocyte syndrome (BLS), is a disease of gene regulation. Patients with BLS have been classified into at least three complementation groups (A, B, and C) believed to correspond to three distinct MHC class II regulatory genes. The elucidation of the molecular basis for this disease will thus clarify the mechanisms controlling the complex regulation of MHC class II genes. Complementation groups B and C are characterized by a lack of binding of RFX, a nuclear protein that normally binds specifically to the X box cis-acting elem

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Durand, B., M. Kobr, W. Reith, and B. Mach. "Functional complementation of major histocompatibility complex class II regulatory mutants by the purified X-box-binding protein RFX." Molecular and Cellular Biology 14, no. 10 (1994): 6839–47. http://dx.doi.org/10.1128/mcb.14.10.6839-6847.1994.

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Major histocompatibility complex (MHC) class II deficiency, or bare lymphocyte syndrome (BLS), is a disease of gene regulation. Patients with BLS have been classified into at least three complementation groups (A, B, and C) believed to correspond to three distinct MHC class II regulatory genes. The elucidation of the molecular basis for this disease will thus clarify the mechanisms controlling the complex regulation of MHC class II genes. Complementation groups B and C are characterized by a lack of binding of RFX, a nuclear protein that normally binds specifically to the X box cis-acting elem

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Trgovcich, Joanne, David Johnson та Bernard Roizman. "Cell Surface Major Histocompatibility Complex Class II Proteins Are Regulated by the Products of the γ134.5 and UL41 Genes of Herpes Simplex Virus 1". Journal of Virology 76, № 14 (2002): 6974–86. http://dx.doi.org/10.1128/jvi.76.14.6974-6986.2002.

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ABSTRACT Modulation of host immune responses has emerged as a common strategy employed by herpesviruses both to establish life-long infections and to affect recovery from infection. Herpes simplex virus 1 (HSV-1) blocks the major histocompatibility complex (MHC) class I antigen presentation pathway by inhibiting peptide transport into the endoplasmic reticulum. The interaction of viral gene products with the MHC class II pathway, however, has not been thoroughly investigated, although CD4+ T cells play an important role in human recovery from infection. We have investigated the stability, dist

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Kretsovali, Androniki, Theodora Agalioti, Charalambos Spilianakis, Eleni Tzortzakaki, Menie Merika, and Joseph Papamatheakis. "Involvement of CREB Binding Protein in Expression of Major Histocompatibility Complex Class II Genes via Interaction with the Class II Transactivator." Molecular and Cellular Biology 18, no. 11 (1998): 6777–83. http://dx.doi.org/10.1128/mcb.18.11.6777.

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ABSTRACT The class II transactivator (CIITA) is a key regulatory factor that controls expression of the major histocompatibility complex (MHC) class II genes that are essential components for antigen presentation and thus regulation of the immune response. We show here that the adenovirus E1A protein interferes with the action of CIITA and inhibits both B-cell-specific and gamma interferon (IFN-γ)-induced expression of MHC class II promoters. Transfection studies provide evidence for the functional role of the CREB-binding protein (CBP) in IFN-γ and CIITA-mediated MHC class II promoter activat

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Gabrilovich, Dmitry. "Mechanism of Myeloid-Derived Suppressor Cell Differentiation in Cancer." Blood 114, no. 22 (2009): SCI—31—SCI—31. http://dx.doi.org/10.1182/blood.v114.22.sci-31.sci-31.

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Abstract Abstract SCI-31 Myeloid-derived suppressor cells (MDSC) represent an intrinsic part of myeloid cell lineage and comprised of myeloid progenitors and precursors of myeloid cells. In healthy host upon generation in bone marrow immature myeloid cells (IMC) quickly differentiate into mature granulocytes, macrophages, or dendritic cells. In a number of pathological conditions (cancer, various infections diseases, sepsis, trauma, bone marrow transplantation, autoimmune abnormalities) increased production of IMC is associated with partial block of their differentiation and most importantly p

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Tze, Lina E., Keisuke Horikawa, Heather Domaschenz, et al. "CD83 increases MHC II and CD86 on dendritic cells by opposing IL-10–driven MARCH1-mediated ubiquitination and degradation." Journal of Experimental Medicine 208, no. 1 (2011): 149–65. http://dx.doi.org/10.1084/jem.20092203.

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Effective vaccine adjuvants must induce expression of major histocompatability (MHC) class II proteins and the costimulatory molecule CD86 on dendritic cells (DCs). However, some adjuvants elicit production of cytokines resulting in adverse inflammatory consequences. Development of agents that selectively increase MHC class II and CD86 expression without triggering unwanted cytokine production requires a better understanding of the molecular mechanisms influencing the production and degradation of MHC class II and CD86 in DCs. Here, we investigate how CD83, an immunoglobulin protein expressed

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SWAIN, MARTIN T., ANTHONY J. BROOKS, and GRAHAM J. L. KEMP. "PREDICTING PEPTIDE INTERACTIONS WITH MODEL CLASS II MHC STRUCTURES." International Journal on Artificial Intelligence Tools 14, no. 04 (2005): 561–75. http://dx.doi.org/10.1142/s0218213005002260.

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An automated method for constructing 3D models of class II MHC structures that uses constraint logic programming to select side-chain conformations is described. This method follows a comparative modeling approach in basing the model structures on experimentally determined MHC-peptide structures, but it uses constraints to ease open the peptide binding groove so that the modeled MHC structure is a less specific fit for the co-crystallized peptide in the starting structure. The resulting models are used by a "peptide threading" program that attempts to predict peptides from a protein sequence t

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Doucet, Jean-Daniel, Marie-Andrée Forget, Cécile Grange, et al. "Endogenously expressed matrix protein M1 and nucleoprotein of influenza A are efficiently presented by class I and class II major histocompatibility complexes." Journal of General Virology 92, no. 5 (2011): 1162–71. http://dx.doi.org/10.1099/vir.0.029777-0.

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Current influenza vaccines containing primarily hypervariable haemagglutinin and neuraminidase proteins must be prepared against frequent new antigenic variants. Therefore, there is an ongoing effort to develop influenza vaccines that also elicit strong and sustained cytotoxic responses against highly conserved determinants such as the matrix (M1) protein and nucleoprotein (NP). However, their antigenic presentation properties in humans are less defined. Accordingly, we analysed MHC class I and class II presentation of endogenously processed M1 and NP in human antigen presenting cells and obse

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