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Journal articles on the topic 'Major histocompatibility complex class II (MHC-II)'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Stosik, Michał, Beata Tokarz-Deptuła, and Wiesław Deptuła. "Major histocompatibility complex in Osteichthyes." Journal of Veterinary Research 64, no. 1 (2020): 127–36. http://dx.doi.org/10.2478/jvetres-2020-0025.

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AbstractBased on analysis of available genome sequences, five gene lineages of MHC class I molecules (MHC I-U, -Z, -S, -L and -P) and one gene lineage of MHC class II molecules (MHC II-D) have been identified in Osteichthyes. In the latter lineage, three MHC II molecule sublineages have been identified (MHC II-A, -B and -E). As regards MHC class I molecules in Osteichthyes, it is important to take note of the fact that the lineages U and Z in MHC I genes have been identified in almost all fish species examined so far. Phylogenetic studies into MHC II molecule genes of sublineages A and B sugge

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Matheux, Franck, and Jean Villard. "Cellular and Gene Therapy for Major Histocompatibility Complex Class II Deficiency." Physiology 19, no. 3 (2004): 154–58. http://dx.doi.org/10.1152/nips.01462.2003.

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Major histocompatibility complex (MHC) class II deficiency is a primary immunodeficiency. Lentiviral vectors are used for gene therapy in a mouse model of this disease. In addition, by a direct genetic correction approach, a diagnostic test to determine which of the four MHC II genes is defective in new MHC II-deficiency patients has been optimized.

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Plasil, Wijkmark, Elbers, Oppelt, Burger, and Horin. "The Major Histocompatibility Complex of Old World Camels—A Synopsis." Cells 8, no. 10 (2019): 1200. http://dx.doi.org/10.3390/cells8101200.

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This study brings new information on major histocompatibility complex (MHC) class III sub-region genes in Old World camels and integrates current knowledge of the MHC region into a comprehensive overview for Old World camels. Out of the MHC class III genes characterized, TNFA and the LY6 gene family showed high levels of conservation, characteristic for MHC class III loci in general. For comparison, an MHC class II gene TAP1, not coding for antigen presenting molecules but functionally related to MHC antigen presenting functions was studied. TAP1 had many SNPs, even higher than the MHC class I

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4

Yamaguchi and Dijkstra. "Major Histocompatibility Complex (MHC) Genes and Disease Resistance in Fish." Cells 8, no. 4 (2019): 378. http://dx.doi.org/10.3390/cells8040378.

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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

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Benichou, G., P. A. Takizawa, P. T. Ho, et al. "Immunogenicity and tolerogenicity of self-major histocompatibility complex peptides." Journal of Experimental Medicine 172, no. 5 (1990): 1341–46. http://dx.doi.org/10.1084/jem.172.5.1341.

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Mechanisms involved in self-antigen processing and presentation are crucial in understanding the induction of self-tolerance in the thymus. We examined the immunogenicity of determinants from major histocompatibility complex (MHC) molecules that are expressed in the thymus and have tested peptides derived from the polymorphic regions of class I and class II molecules. We found that two peptides corresponding to NH2 termini of the class II alpha and beta chains (Ak alpha 1-18 and Ak beta 1-16) could bind to self-Ak molecules with high affinity and, surprisingly, were immunogenic in that they co

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6

De Oliveira Andrade, Luis Jesuino, Paulo Roberto Santana de Melo, Larissa Santos França, Luciana Santos França, Ana Micheline Andrade Malta, and Raymundo Paraná. "Human major histocompatibility complex and thyroid dysfunction in hepatitis C carries." Revista de Ciências Médicas e Biológicas 10, no. 2 (2011): 179. http://dx.doi.org/10.9771/cmbio.v10i2.4825.

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The major histocompatibility complex (MHC) is a multigene family of receptors which are crucial in antigen presentation, mediation, and initiation of the cellular immune response. An association exists between certain MHC polymorphisms and autoimmune thyroid disease in animals and humans. Hepatitis C virus (HCV) infection has been shown to be associated with increased incidence of thyroid dysfunction, moreover, interferon-á (IFN-á) therapy of chronic HCV infection is associated with the thyroid dysfunction. IFN-á has been the basis for the treatment of HCV infection has been identified as an i

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7

Woods, A., H. Y. Chen, M. E. Trumbauer, A. Sirotina, R. Cummings, and D. M. Zaller. "Human major histocompatibility complex class II-restricted T cell responses in transgenic mice." Journal of Experimental Medicine 180, no. 1 (1994): 173–81. http://dx.doi.org/10.1084/jem.180.1.173.

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Transgenic mice expressing human major histocompatibility complex (MHC) class II molecules would provide a valuable model system for studying human immunology. However, attempts to obtain human class II-restricted T cell responses in such transgenic mice have had only limited success, possibly due to an inability of mouse CD4 to interact efficiently with human MHC class II molecules. To circumvent this problem, we constructed recombinant MHC class II genes in which the peptide-binding domain was derived from human DR sequences whereas the CD4-binding domain was derived from mouse I-E sequences

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Slobedman, Barry, Edward S. Mocarski, Ann M. Arvin, Elizabeth D. Mellins, and Allison Abendroth. "Latent cytomegalovirus down-regulates major histocompatibility complex class II expression on myeloid progenitors." Blood 100, no. 8 (2002): 2867–73. http://dx.doi.org/10.1182/blood.v100.8.2867.

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Following primary infection, human cytomegalovirus (CMV) establishes a lifelong latent infection in bone marrow–derived myeloid lineage cells. Although downmodulation of major histocompatibility complex (MHC) class I and class II protein levels occurs during active viral replication, little is known about the modulation of these proteins during latent infection. When analyzed by flow cytometry, latently infected adherent cells collected from granulocyte macrophage progenitor (GM-P) cultures exhibited a striking reduction in MHC class II antigen present on the cell surface starting very early a

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9

Massa, P. T. "Specific suppression of major histocompatibility complex class I and class II genes in astrocytes by brain-enriched gangliosides." Journal of Experimental Medicine 178, no. 4 (1993): 1357–63. http://dx.doi.org/10.1084/jem.178.4.1357.

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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 g

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Plaeger-Marshall, Susan, Albert Haas, Loran T. Clement, et al. "Interferon-induced expression of class II major histocompatibility antigens in the major histocompatibility complex (MHC) class II deficiency syndrome." Journal of Clinical Immunology 8, no. 4 (1988): 285–95. http://dx.doi.org/10.1007/bf00916557.

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11

Morkowski, S., A. W. Goldrath, S. Eastman, et al. "T cell recognition of major histocompatibility complex class II complexes with invariant chain processing intermediates." Journal of Experimental Medicine 182, no. 5 (1995): 1403–13. http://dx.doi.org/10.1084/jem.182.5.1403.

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Peptides from the lumenal portion of invariant chain (Ii) spanning residues 80-106 (class II-associated Ii peptide [CLIP]) are found in association with several mouse and human major histocompatibility complex (MHC) class II allelic variants in wild-type and presentation-deficient mutant cells. The ready detection of these complexes suggests that such an intermediate is essential to the MHC class II processing pathway. In this study, we demonstrate that T cells recognize CLIP/MHC class II complexes on the surface of normal and mutant cells in a manner indistinguishable from that of nominal ant

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12

Hermsen, Eden M., Lauren J. Young, and Julie M. Old. "Major Histocompatibility Complex Class II in the red-tailed phascogale (Phascogale calura)." Australian Mammalogy 39, no. 1 (2017): 28. http://dx.doi.org/10.1071/am16002.

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Diversity in major histocompatibility complex (MHC) genes can be correlated with the level of immunological fitness of an individual or group of individuals. This study tested published primer sets designed to amplify fragments of the MHC Class II DAB and DBB genes to amplify the equivalent gene fragments in red-tailed phascogales (Phascogale calura). Seventeen genomic DNA samples extracted from phascogale muscle tissue were used to amplify the initial DAB and DBB fragments; however, only DAB PCR proved successful. The fragments were 172 bp in length between the primers and had a high level of

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13

Jevnikar, A. M., M. J. Grusby, and L. H. Glimcher. "Prevention of nephritis in major histocompatibility complex class II-deficient MRL-lpr mice." Journal of Experimental Medicine 179, no. 4 (1994): 1137–43. http://dx.doi.org/10.1084/jem.179.4.1137.

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MRL-lpr mice develop aggressive autoimmune kidney disease associated with increased or de novo renal expression of major histocompatibility complex (MHC) class II molecules and a massive systemic expansion of CD4-CD- double negative (DN) T cells. Whereas non-MHC linked genes can have a profound effect on the development of nephritis, lymphadenopathy, and anti-DNA antibody production in MRL-lpr mice, the role of MHC molecules has not been unequivocally established. To study the role of MHC class II in this murine model of systemic lupus erythematosis, class II-deficient MRL-lpr mice (MRL-lpr -/

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14

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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15

Bosshart, Herbert, and Ruth F. Jarrett. "Deficient Major Histocompatibility Complex Class II Antigen Presentation in a Subset of Hodgkin's Disease Tumor Cells." Blood 92, no. 7 (1998): 2252–59. http://dx.doi.org/10.1182/blood.v92.7.2252.

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Abstract Hodgkin's disease is a common malignancy of the lymphoid system. Although the scarce Hodgkin and Reed-Sternberg (HRS) tumor cells in involved tissue synthesize major histocompatibility complex (MHC) class II and costimulatory molecules such as CD40 or CD86, it is unclear whether these tumor cells are operational antigen-presenting cells (APC). We developed an immunofluorescence-based assay to determine the number of MHC class II molecules present on the surface of single living HRS cells. We found that in fresh Hodgkin's disease lymph node biopsies, a subset of HRS cells express a sub

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Bosshart, Herbert, and Ruth F. Jarrett. "Deficient Major Histocompatibility Complex Class II Antigen Presentation in a Subset of Hodgkin's Disease Tumor Cells." Blood 92, no. 7 (1998): 2252–59. http://dx.doi.org/10.1182/blood.v92.7.2252.2252_2252_2259.

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Hodgkin's disease is a common malignancy of the lymphoid system. Although the scarce Hodgkin and Reed-Sternberg (HRS) tumor cells in involved tissue synthesize major histocompatibility complex (MHC) class II and costimulatory molecules such as CD40 or CD86, it is unclear whether these tumor cells are operational antigen-presenting cells (APC). We developed an immunofluorescence-based assay to determine the number of MHC class II molecules present on the surface of single living HRS cells. We found that in fresh Hodgkin's disease lymph node biopsies, a subset of HRS cells express a substantial

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17

Majumder, Parimal, and Jeremy M. Boss. "CTCF Controls Expression and Chromatin Architecture of the Human Major Histocompatibility Complex Class II Locus." Molecular and Cellular Biology 30, no. 17 (2010): 4211–23. http://dx.doi.org/10.1128/mcb.00327-10.

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ABSTRACT The major histocompatibility complex class II (MHC-II) locus includes a dense cluster of genes that function to initiate immune responses. Expression of insulator CCCTC binding factor (CTCF) was found to be required for expression of all MHC class II genes associated with antigen presentation. Ten CTCF sites that divide the MHC-II locus into apparent evolutionary domains were identified. To define the role of CTCF in mediating regulation of the MHC II genes, chromatin conformation capture assays, which provide an architectural assessment of a locus, were conducted across the MHC-II re

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Chou, Chih-Ling, and Scheherazade Sadegh-Nasseri. "Hla-Dm Recognizes the Flexible Conformation of Major Histocompatibility Complex Class II." Journal of Experimental Medicine 192, no. 12 (2000): 1697–706. http://dx.doi.org/10.1084/jem.192.12.1697.

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DM facilitates formation of high affinity complexes of peptide–major histocompatibility complex (MHC) by release of class II MHC–associated invariant chain peptide (CLIP). This has been proposed to occur through discrimination of complex stability. By probing kinetic and conformational intermediates of the wild-type and mutant human histocompatibility leukocyte antigen (HLA)-DR1–peptide complexes, and examining their reactivities with DM, we propose that DM interacts with the flexible hydrophobic pocket 1 of DR1 and converts the molecule into a conformation that is highly peptide receptive. A

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19

O, Eunju, Young-Tae Lee, Eun-Ju Ko, et al. "Roles of Major Histocompatibility Complex Class II in Inducing Protective Immune Responses to Influenza Vaccination." Journal of Virology 88, no. 14 (2014): 7764–75. http://dx.doi.org/10.1128/jvi.00748-14.

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ABSTRACTMajor histocompatibility complex class II-deficient (MHC-II KO; Aβ−/−) mice were used to assess the roles of MHC-II molecules in inducing protective immune responses to vaccination. After vaccination with influenza A/PR8 virus-like particle (VLP) vaccine,in vivoandin vitrovaccine antigen-specific IgG isotype antibodies were not detected in MHC-II KO mice, which is quite different from CD4 T cell-deficient mice that induced vaccine-specific IgG antibodies. The deficiency in MHC-II did not significantly affect the induction of antigen-specific IgM antibody in sera. MHC-II KO mice that we

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Schmidt, Dennis, Joan Verdaguer, Nuzhat Averill, and Pere Santamaria. "A Mechanism for the Major Histocompatibility Complex–linked Resistance to Autoimmunity." Journal of Experimental Medicine 186, no. 7 (1997): 1059–75. http://dx.doi.org/10.1084/jem.186.7.1059.

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Certain major histocompatibility complex (MHC) class II haplotypes encode elements providing either susceptibility or dominant resistance to the development of spontaneous autoimmune diseases via mechanisms that remain undefined. Here we show that a pancreatic beta cell–reactive, I-Ag7–restricted, transgenic TCR that is highly diabetogenic in nonobese diabetic mice (H-2g7) undergoes thymocyte negative selection in diabetes-resistant H-2g7/b, H-2g7/k, H-2g7/q, and H-2g7/nb1 NOD mice by engaging antidiabetogenic MHC class II molecules on thymic bone marrow–derived cells, independently of endogen

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Gaseitsiwe, Simani, Davide Valentini, Raija Ahmed, et al. "Major Histocompatibility Complex Class II Molecule-Human Immunodeficiency Virus Peptide Analysis Using a Microarray Chip." Clinical and Vaccine Immunology 16, no. 4 (2009): 567–73. http://dx.doi.org/10.1128/cvi.00441-08.

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ABSTRACT Identification of major histocompatibility complex (MHC) class II binding peptides is a crucial step in rational vaccine design and immune monitoring. We designed a novel MHC class II molecule-peptide microarray binding assay and evaluated 346 peptides from already identified human immunodeficiency virus (HIV) epitopes and an additional set (n = 206) of 20-mer peptides, overlapping by 15 amino acid residues, from HIV type 1B (HIV-1B) gp160 and Nef as a paradigm. Peptides were attached via the N-terminal part to a linker that covalently binds to the epoxy glass slide. The 552 peptides

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22

Li, Shuo, Christian Kurts, Frank Köntgen, Stephen R. Holdsworth, and Peter G. Tipping. "Major Histocompatibility Complex Class II Expression by Intrinsic Renal Cells Is Required for Crescentic Glomerulonephritis." Journal of Experimental Medicine 188, no. 3 (1998): 597–602. http://dx.doi.org/10.1084/jem.188.3.597.

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The requirement for major histocompatibility complex class II (MHC II) to initiate immune renal injury was studied in a murine model of CD4+ T cell–dependent crescentic glomerulonephritis (GN). C57BL/6 (MHC II+/+) mice developed crescentic GN with glomerular CD4+ T cell infiltration and renal injury, in response to a nephritogenic antigen (sheep globulin) planted on their glomerular basement membrane. MHC II–deficient C57BL/6 mice (MHC II−/−) did not develop crescentic GN, CD4+ T cell infiltration, or injury, indicating that this form of immune glomerular injury is MHC II dependent. The requir

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Pappo, Jacques, Deirdre Torrey, Lillian Castriotta, Anneli Savinainen, Zita Kabok, and Alexander Ibraghimov. "Helicobacter pylori Infection in Immunized Mice Lacking Major Histocompatibility Complex Class I and Class II Functions." Infection and Immunity 67, no. 1 (1999): 337–41. http://dx.doi.org/10.1128/iai.67.1.337-341.1999.

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ABSTRACT The role of major histocompatibility complex (MHC) class I- and class II-restricted functions in Helicobacter pyloriinfection and immunity upon oral immunization was examined in vivo. Experimental challenge with H. pylori SS1 resulted in significantly greater (P ≤ 0.025) colonization of MHC class I and class II mutant mice than C57BL/6 wild-type mice. Oral immunization with H. pylori whole-cell lysates and cholera toxin adjuvant significantly reduced the magnitude of H. pylori infection in C57BL/6 wild-type (P = 0.0083) and MHC class I knockout mice (P = 0.0048), but it had no effect

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Peters, P. J., G. Raposo, J. J. Neefjes, et al. "Major histocompatibility complex class II compartments in human B lymphoblastoid cells are distinct from early endosomes." Journal of Experimental Medicine 182, no. 2 (1995): 325–34. http://dx.doi.org/10.1084/jem.182.2.325.

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In human B lymphoblastoid cell lines, the majority of major histocompatibility complex (MHC) class II heterodimers are located on the cell surface and in endocytic compartments, while invariant chain (Ii)-associated class II molecules represent biosynthetic intermediates which are present mostly in the endoplasmic reticulum and Golgi complex. To investigate the origin of the MHC class II-positive compartments and their relation to early endosomes, the intracellular distribution of MHC class II molecules and Ii in relation to endocytic tracers was studied in human lymphoblastoid B cells by immu

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Chang, C. H., W. L. Fodor, and R. A. Flavell. "Reactivation of a major histocompatibility complex class II gene in mouse plasmacytoma cells and mouse T cells." Journal of Experimental Medicine 176, no. 5 (1992): 1465–69. http://dx.doi.org/10.1084/jem.176.5.1465.

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Terminally differentiated plasma cells and mouse T cells do not express major histocompatibility complex (MHC) class II genes although class II gene expression is observed in pre-B and mature B cells as well as in activated human T cells. Transient heterokaryons were prepared and analyzed to investigate the mechanisms of inactivation of MHC class II gene in mouse plasmacytoma cells and mouse T cells. The endogenous MHC class II genes in both mouse plasmacytoma cells and mouse T cells can be reactivated by factors present in B cells. This reactivation of class II gene is also observed by fusion

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Brocker, Thomas. "Survival of Mature CD4 T Lymphocytes Is Dependent on Major Histocompatibility Complex Class II–expressing Dendritic Cells." Journal of Experimental Medicine 186, no. 8 (1997): 1223–32. http://dx.doi.org/10.1084/jem.186.8.1223.

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Thymic T cell development is controlled by T cell receptor (TCR)–major histocompatibility complex (MHC) interactions, whereas a further dependence of peripheral mature T cells on TCR–MHC contact has not been described so far. To study this question, CD4 T cell survival was surveyed in mice lacking MHC class II expression and in mice expressing MHC class II exclusively on dendritic cells. Since neither of these mice positively select CD4 T cells in the thymus, they were grafted with MHC class II–positive embryonic thymic tissue, which had been depleted of bone marrow derived cells. Although the

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Donaldson, W. L., C. H. Zhang, J. G. Oriol, and D. F. Antczak. "Invasive equine trophoblast expresses conventional class I major histocompatibility complex antigens." Development 110, no. 1 (1990): 63–71. http://dx.doi.org/10.1242/dev.110.1.63.

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Monoclonal antibodies and alloantisera were used in an indirect immunohistochemical assay to determine the expression of class I and class II Major Histocompatibility Complex (MHC) antigens by equine placental cells and the endometrial tissues at the fetal-maternal interface. MHC class I antigens were expressed at high density on the surface of the trophoblast cells of the chorionic girdle at days 32–36, just prior to their invasion of the endometrium. The mature gonadotrophin-secreting cells of the endometrial cups, which are derived from the chorionic girdle cells, had greatly reduced levels

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Ulbricht, Tobias, Mohammad Alzrigat, Almut Horch, et al. "PML promotes MHC class II gene expression by stabilizing the class II transactivator." Journal of Cell Biology 199, no. 1 (2012): 49–63. http://dx.doi.org/10.1083/jcb.201112015.

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Promyelocytic leukemia (PML) nuclear bodies selectively associate with transcriptionally active genomic regions, including the gene-rich major histocompatibility (MHC) locus. In this paper, we have explored potential links between PML and interferon (IFN)-γ–induced MHC class II expression. IFN-γ induced a substantial increase in the spatial proximity between PML bodies and the MHC class II gene cluster in different human cell types. Knockdown experiments show that PML is required for efficient IFN-γ–induced MHC II gene transcription through regulation of the class II transactivator (CIITA). PM

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Lankar, Danielle, Hélène Vincent-Schneider, Volker Briken, Takeaki Yokozeki, Graça Raposo, and Christian Bonnerot. "Dynamics of Major Histocompatibility Complex Class II Compartments during B Cell Receptor–mediated Cell Activation." Journal of Experimental Medicine 195, no. 4 (2002): 461–72. http://dx.doi.org/10.1084/jem.20011543.

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Antigen recognition by clonotypic B cell receptor (BcR) is the first step of B lymphocytes differentiation into plasmocytes. This B cell function is dependent on efficient major histocompatibility complex (MHC) class II–restricted presentation of BcR-bound antigens. In this work, we analyzed the subcellular mechanisms underlying antigen presentation after BcR engagement on B cells. In quiescent B cells, we found that MHC class II molecules mostly accumulated at the cell surface and in an intracellular pool of tubulovesicular structures, whereas H2-M molecules were mostly detected in distinct l

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Kleijmeer, Monique J., Stanislaw Morkowski, Janice M. Griffith, Alexander Y. Rudensky, and Hans J. Geuze. "Major Histocompatibility Complex Class II Compartments in Human and Mouse B Lymphoblasts Represent Conventional Endocytic Compartments." Journal of Cell Biology 139, no. 3 (1997): 639–49. http://dx.doi.org/10.1083/jcb.139.3.639.

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In most human and mouse antigen-presenting cells, the majority of intracellular major histocompatibility complex (MHC) class II molecules resides in late endocytic MHC class II compartments (MIICs), thought to function in antigen processing and peptide loading. However, in mouse A20 B cells, early endocytic class II-containing vesicles (CIIVs) have been reported to contain most of the intracellular MHC class II molecules and have also been implicated in formation of MHC class II–peptide complexes. To address this discrepancy, we have studied in great detail the endocytic pathways of both a hum

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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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Giuliani, Cesidio, Ines Bucci, Valeria Montani, et al. "Regulation of major histocompatibility complex gene expression in thyroid epithelial cells by methimazole and phenylmethimazole." Journal of Endocrinology 204, no. 1 (2009): 57–66. http://dx.doi.org/10.1677/joe-09-0172.

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Increased expression of major histocompatibility complex (MHC) class-I genes and aberrant expression of MHC class-II genes in thyroid epithelial cells (TECs) are associated with autoimmune thyroid diseases. Previous studies have shown that methimazole (MMI) reduces MHC class-I expression and inhibits interferon-γ (IFN-γ or IFNG as listed in the MGI Database)-induced expression of the MHC class-II genes in TECs. The action of MMI on the MHC class-I genes is transcriptional, but its mechanism has not been investigated previously. In the present study, we show that in Fisher rat thyroid cell line

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Nikolic-Paterson, D. J., G. H. Tesch, H. Y. Lan, R. Foti, and R. C. Atkins. "Deoxyspergualin inhibits mesangial cell proliferation and major histocompatibility complex class II expression." Journal of the American Society of Nephrology 5, no. 11 (1995): 1895–902. http://dx.doi.org/10.1681/asn.v5111895.

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It has previously been shown that the immunosuppressive drug deoxyspergualin can inhibit renal injury in experimental glomerulonephritis. This study examined whether deoxyspergualin can modulate the mesangial cell response to glomerular injury. Antiglomerular basement membrane glomerulonephritis was induced in primed rats. Groups of five animals were treated with deoxyspergualin (5 mg/kg per day) or saline from Day 0 until being euthanized on Day 1, 7, 14, or 21. Deoxyspergualin treatment significantly inhibited mesangial cell proliferation (proliferating cell nuclear antigen expression) over

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Mudhasani, Rajini, and Joseph D. Fontes. "The Class II Transactivator Requires brahma-Related Gene 1 To Activate Transcription of Major Histocompatibility Complex Class II Genes." Molecular and Cellular Biology 22, no. 14 (2002): 5019–26. http://dx.doi.org/10.1128/mcb.22.14.5019-5026.2002.

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ABSTRACT The class II transactivator (CIITA) is the key regulator of major histocompatibility complex (MHC) class II gene transcription. We demonstrate here that CIITA requires the ATPase subunit of an hSWI/SNF complex, brahma-related gene 1 (BRG-1), to activate transcription. When introduced into a cell line lacking BRG-1, CIITA was unable to activate cellular MHC class II genes. Reexpression of the wild-type but not an ATP-binding-deficient BRG-1 protein in this cell line restored the ability of CIITA to transactivate transcription of MHC class II genes. Interestingly, when the activity of C

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Olsén, Arne, Mary Jo Wick, Matthias Mörgelin, and Lars Björck. "Curli, Fibrous Surface Proteins ofEscherichia coli, Interact with Major Histocompatibility Complex Class I Molecules." Infection and Immunity 66, no. 3 (1998): 944–49. http://dx.doi.org/10.1128/iai.66.3.944-949.1998.

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ABSTRACT Curli are thin, coiled fibers expressed on the surface ofEscherichia coli that bind several matrix and plasma proteins such as fibronectin, laminin, plasminogen, tissue plasminogen activator, and H-kininogen. In this work, we examined the interactions between curli-expressing E. coli and human major histocompatibility complex class I (MHC-I) and class II (MHC-II) molecules. Curliated E. coli was found to interact with an MHC-I-expressing lymphoma cell line as shown by scanning electron microscopy, whereas the binding to a mutant variant of this cell line expressing small amounts of MH

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Shi, Guo-Ping, Rebecca A. R. Bryant, Richard Riese, et al. "Role for Cathepsin F in Invariant Chain Processing and Major Histocompatibility Complex Class II Peptide Loading by Macrophages." Journal of Experimental Medicine 191, no. 7 (2000): 1177–86. http://dx.doi.org/10.1084/jem.191.7.1177.

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The major histocompatibility complex (MHC) class II–associated invariant chain (Ii) regulates intracellular trafficking and peptide loading of MHC class II molecules. Such loading occurs after endosomal degradation of the invariant chain to a ∼3-kD peptide termed CLIP (class II–associated invariant chain peptide). Cathepsins L and S have both been implicated in degradation of Ii to CLIP in thymus and peripheral lymphoid organs, respectively. However, macrophages from mice deficient in both cathepsins S and L can process Ii and load peptides onto MHC class II dimers normally. Both processes are

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Mellins, E., S. Kempin, L. Smith, T. Monji, and D. Pious. "A gene required for class II-restricted antigen presentation maps to the major histocompatibility complex." Journal of Experimental Medicine 174, no. 6 (1991): 1607–15. http://dx.doi.org/10.1084/jem.174.6.1607.

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We have previously described a set of mutants (16.23-selected mutants) of a B lymphoblastoid cell line that are defective in the presentation of intact proteins to class II-restricted T cells, but effectively present immunogenic peptides. The mutations in these mutants are recessive in somatic cell hybrids and are not in Class II structural genes. Here, we report on a unique mutant, 5.2.4, in which a similar defect in class II-restricted antigen presentation has occurred in association with a one-megabase homozygous deletion in the class II region of the major histocompatibility complex (MHC).

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Brachet, Valérie, Gérard Péhau-Arnaudet, Catherine Desaymard, Graça Raposo, and Sebastian Amigorena. "Early Endosomes Are Required for Major Histocompatiblity Complex Class II Transport to Peptide-loading Compartments." Molecular Biology of the Cell 10, no. 9 (1999): 2891–904. http://dx.doi.org/10.1091/mbc.10.9.2891.

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Antigen presentation to CD4+ T lymphocytes requires transport of newly synthesized major histocompatibility complex (MHC) class II molecules to the endocytic pathway, where peptide loading occurs. This step is mediated by a signal located in the cytoplasmic tail of the MHC class II-associated Ii chain, which directs the MHC class II-Ii complexes from the trans-Golgi network (TGN) to endosomes. The subcellular machinery responsible for the specific targeting of MHC class II molecules to the endocytic pathway, as well as the first compartments these molecules enter after exit from the TGN, remai

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van der Wel, Nicole N., Masahiko Sugita, Donna M. Fluitsma, et al. "CD1 and Major Histocompatibility Complex II Molecules Follow a Different Course during Dendritic Cell Maturation." Molecular Biology of the Cell 14, no. 8 (2003): 3378–88. http://dx.doi.org/10.1091/mbc.e02-11-0744.

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The maturation of dendritic cells is accompanied by the redistribution of major histocompatibility complex (MHC) class II molecules from the lysosomal MHC class II compartment to the plasma membrane to mediate presentation of peptide antigens. Besides MHC molecules, dendritic cells also express CD1 molecules that mediate presentation of lipid antigens. Herein, we show that in human monocyte-derived dendritic cells, unlike MHC class II, the steady-state distribution of lysosomal CD1b and CD1c isoforms was unperturbed in response to lipopolysaccharide-induced maturation. However, the lysosomes i

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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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Ellerman, K. E., and A. A. Like. "A major histocompatibility complex class II restriction for BioBreeding/Worcester diabetes-inducing T cells." Journal of Experimental Medicine 182, no. 4 (1995): 923–30. http://dx.doi.org/10.1084/jem.182.4.923.

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Inbred diabetes-prone (DP) BioBreeding/Worcester (BB/Wor) (RT1u) rats develop spontaneous autoimmune diabetes, which, like human insulin-dependent diabetes mellitus, is mediated by autoreactive T lymphocytes. Breeding studies have shown an absolute requirement for at least one copy of the major histocompatibility complex (MHC) RT1u haplotype for spontaneous diabetes expression. Concanavalin A-activated spleen cells from acutely diabetic DP rats adoptively transfer diabetes only to recipients that express at least one RT1u haplotype. To investigate the basis for the MHC requirement in BB/Wor au

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Abd El Halim, Zeinab, Amr Badr, Khaled Tawfik, and Ibrahim Farag. "Major Histocompatibility Complex Class II Prediction." American Journal of Bioinformatics Research 2, no. 1 (2012): 14–20. http://dx.doi.org/10.5923/j.bioinformatics.20120201.03.

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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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Chang, C. H., and R. A. Flavell. "Class II transactivator regulates the expression of multiple genes involved in antigen presentation." Journal of Experimental Medicine 181, no. 2 (1995): 765–67. http://dx.doi.org/10.1084/jem.181.2.765.

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CIITA (a major histocompatibility complex [MHC] class II transactivator) has been shown to be required for the expression of MHC class II genes in both B cells and interferon gamma-inducible cells. Here we demonstrate that CIITA not only activates MHC class II genes but also genes required for antigen presentation. Mutant HeLa cells, defective in the expression of classic MHC class II genes, invariant chain, and the newly described human histocompatibility leukocyte antigen-DM genes, were used to study the role of CIITA in the regulation of these genes. Upon transfection with CIITA cDNA, the m

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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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Silacci, P., A. Mottet, V. Steimle, W. Reith, and B. Mach. "Developmental extinction of major histocompatibility complex class II gene expression in plasmocytes is mediated by silencing of the transactivator gene CIITA." Journal of Experimental Medicine 180, no. 4 (1994): 1329–36. http://dx.doi.org/10.1084/jem.180.4.1329.

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Constitutive major histocompatibility complex (MHC) class II gene expression is tightly restricted to antigen presenting cells and is under developmental control. Cells of the B cell lineage acquire the capacity to express MHC class II genes early during ontogeny and lose this property during terminal differentiation into plasma cells. Cell fusion experiments have suggested that the extinction of MHC class II expression in plasma cells is due to a dominant repression, but the underlying mechanisms are not understood. CIITA was recently identified as an MHC class II transactivator that is essen

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Mukherjee, R., Z. Zhang, R. Zhong, Z. Q. Yin, D. C. Roopenian, and A. M. Jevnikar. "Lupus nephritis in the absence of renal major histocompatibility complex class I and class II molecules." Journal of the American Society of Nephrology 7, no. 11 (1996): 2445–52. http://dx.doi.org/10.1681/asn.v7112445.

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MRL/Mp-lpr/lpr (MRL-lpr) mice develop an aggressive autoimmune disorder characterized by arthritis, vasculitis, and glomerulonephritis. Renal injury is associated with increased expression of major histocompatibility complex (MHC) molecules, as well as cytokines, adhesion molecules (intracellular adhesion molecule-1, vascular cell adhesion molecule-1), and autoantibodies. By using either MHC Class I (MRL-lpr B2m-/-) or MHC Class II deficient (MRL-lpr Ab-/-) kidneys in a transplant model, we tested the role of renal expression of these molecules in the development of autoimmune renal injury. Ki

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Cannon, Matthew J., John S. Davis, and Joy L. Pate. "The class II major histocompatibility complex molecule BoLA-DR is expressed by endothelial cells of the bovine corpus luteum." Reproduction 133, no. 5 (2007): 991–1003. http://dx.doi.org/10.1530/rep-06-0362.

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Cells expressing class II major histocompatibility complex (MHC) molecules are found within the corpus luteum (CL) of several species. Expression and localization of class II MHC molecules in the bovine CL were examined in the present study. Immunohistochemical evaluation revealed class II MHC molecules on single cells in early CL (days 4 and 5 post-estrus). Two class II MHC-expressing cell types were observed in midcycle CL (days 10–12 post-estrus), single cells similar to those observed in the early CL, and endothelial cells. Not all endothelial cells expressed class II MHC, and further inve

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Zhong, Guangming, Tao Fan та Li Liu. "Chlamydia Inhibits Interferon γ–inducible Major Histocompatibility Complex Class II Expression by Degradation of Upstream Stimulatory Factor 1". Journal of Experimental Medicine 189, № 12 (1999): 1931–38. http://dx.doi.org/10.1084/jem.189.12.1931.

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We report that chlamydiae, which are obligate intracellular bacterial pathogens, can inhibit interferon (IFN)-γ–inducible major histocompatibility complex (MHC) class II expression. However, the IFN-γ–induced IFN regulatory factor-1 (IRF-1) and intercellular adhesion molecule 1 (ICAM-1) expression is not affected, suggesting that chlamydia may selectively target the IFN-γ signaling pathways required for MHC class II expression. Chlamydial inhibition of MHC class II expression is correlated with degradation of upstream stimulatory factor (USF)-1, a constitutively and ubiquitously expressed tran

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Jain, Ayushi, Mehar Chand Sharma, Chitra Sarkar, Rohit Bhatia, Sumit Singh, and Rohini Handa. "Major Histocompatibility Complex Class I and II Detection as a Diagnostic Tool in Idiopathic Inflammatory Myopathies." Archives of Pathology & Laboratory Medicine 131, no. 7 (2007): 1070–76. http://dx.doi.org/10.5858/2007-131-1070-mhccia.

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Abstract Context.—Muscle biopsy is at present the gold standard for the diagnosis of idiopathic inflammatory myopathies (IIMs), which include dermatomyositis, polymyositis, and inclusion body myositis. Currently, there is no definite diagnostic marker that helps in the discrimination of different subgroups of IIMs and the discrimination of IIMs from other clinical and morphologic mimics. Major histocompatibility complex (MHC) class I and II antigens are not expressed on normal muscle fibers. Objective.—To determine the diagnostic utility of MHC class I and II antigen expression on the muscle b

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