Erratum: MHC class I and MHC class II DRB gene variability in wild and captive Bengal tigers (Panthera tigris tigris)

Introduction: Peptides obtained by processing intracellular and extracellular antigens are presented to T cells to stimulate the immune response. This presentation is made by peptide receptors called major histocompatibility complex (MHC) molecules. The regulation mechanisms of MHC molecules, which have similar roles in the immune response, especially at the gene level, have significant differences according to their class. Objective: Class I and class II MHC molecules encoded by MHC genes on the short arm of the sixth chromosome are peptide receptors that stimulate T cell response. These peptides, which will enable the recognition of the antigen from which they originate, are loaded into MHC molecules and presented to T cells. Although the principles of loading and delivering peptides are similar for both molecules, the peptide sources and peptide loading mechanisms are different. In addition, class I molecules are expressed in all nucleated cells while class II molecules are expressed only in Antigen Presentation Cells (APC). These differences; It shows that MHC class I is not expressed by exactly the same transcriptional mechanisms as MHC class II. In our article, we aimed to compare the gene expressions of both classes and reveal their similarities and differences. Discussion and Conclusion: A better understanding of the transcriptional mechanisms of MHC molecules will reveal the role of these molecules in diseases more clearly. In our review, we discussed MHC gene regulation mechanisms with presence of existing informations, which is specific to the MHC class, for contribute to future research. Keywords: MHC class I, MHC class II, MHC gene regulation, promoter, SXY module, transcription

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Identification of MHC class II restricted T-cell-mediated reactivity against MHC class I binding Mycobacterium tuberculosis peptides

Immunology ◽

10.1111/j.1365-2567.2010.03383.x ◽

2011 ◽

Vol 132 (4) ◽

pp. 482-491 ◽

Cited By ~ 18

Author(s):

Mingjun Wang ◽

Sheila T. Tang ◽

Anette Stryhn ◽

Sune Justesen ◽

Mette V. Larsen ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

T Cell ◽

Mhc Class I ◽

Mhc Class Ii ◽

Class Ii ◽

Class I

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Towards a systems understanding of MHC class I and MHC class II antigen presentation

Nature Reviews Immunology ◽

10.1038/nri3084 ◽

2011 ◽

Vol 11 (12) ◽

pp. 823-836 ◽

Cited By ~ 845

Author(s):

Jacques Neefjes ◽

Marlieke L. M. Jongsma ◽

Petra Paul ◽

Oddmund Bakke

Keyword(s):

Antigen Presentation ◽

Mhc Class I ◽

Mhc Class Ii ◽

Class Ii ◽

Class I ◽

Class Ii Antigen ◽

Mhc Class Ii Antigen

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Lymphoid Tumors ofXenopus laeviswith Different Capacities for Growth in Larvae and Adults

Developmental Immunology ◽

10.1155/1994/37392 ◽

1994 ◽

Vol 3 (4) ◽

pp. 297-307 ◽

Cited By ~ 50

Author(s):

Jacques Robert ◽

Chantal Guiet ◽

Louis Du Pasquier

Keyword(s):

Cell Surface ◽

Tumor Cell ◽

Tumor Cells ◽

Mhc Class I ◽

Mhc Class Ii ◽

Cell Lineage ◽

Cell Types ◽

Class Ii ◽

Class I ◽

Specific Marker

Three new lymphoid tumors offering an assortment of variants in terms of MHC class I expressions, MHC class II expression, and Ig gene transcription have been discovered in the amphibianXenopus. One was developed in an individual of the isogenic LG15 clone (LG15/0), one in a frog of the LG15/40 clone (derived from a small egg recombinant of LG15), and one (ff-2) in a maleffsib of the individual in which MAR1, the first lymphoid tumor in Xenopus was found 2 years ago. These tumors developed primarily as thymus outgrowths and were transplantable in histocompatible tadpoles but not in nonhistocompatible hosts. Whereas LG15/0 and LG15/40 tumor cells also grow in adult LG15 frogs, theff-2 tumor, like the MAR1 cell line, is rejected by adultffanimals. Using flow cytometry with fluorescence-labeled antibodies and immunoprecipitation analysis, we could demonstrate that, like MAR1, these three new tumors express on their cell surface lymphopoietic markers recognized by mAbs FIF6 and RC47, as well as T-cell lineage markers recognized by mAbs AM22 (CD8-1ike) and X21.2, but not by immunologobulin (Ig) nor MHC class II molecules. Another lymphocyte-specific marker AM15 is expressed by 15/0 and 15/40 but notff-2 tumor cells. Theff-2 tumor cell expresses MHC class molecule in association withβ2-microglobulin on the surface, 15/40 cells contain cytoplasmic Iαchain that is barely detected at the cell surface by fluocytometry, and 15/0 cells do not synthesize class Iαchain at all. The three new tumors all produce large amounts of IgM mRNA of two different sizes but no Ig protein on the membrane nor in the cytoplasm. All tumor cell types synthesize large amount of Myc mRNA and MHC class I-like transcripts considered to be non classical.

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Mouse Schwann cells activate MHC class I and II restricted T-cell responses, but require external peptide processing for MHC class II presentation

Neurobiology of Disease ◽

10.1016/j.nbd.2009.11.006 ◽

2010 ◽

Vol 37 (2) ◽

pp. 483-490 ◽

Cited By ~ 20

Author(s):

Gerd Meyer zu Hörste ◽

Holger Heidenreich ◽

Anne K. Mausberg ◽

Helmar C. Lehmann ◽

Anneloor L.M.A. ten Asbroek ◽

...

Keyword(s):

T Cell ◽

Schwann Cells ◽

Mhc Class I ◽

Mhc Class Ii ◽

T Cell Responses ◽

Class Ii ◽

Class I ◽

Peptide Processing ◽

Cell Responses

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Expression of MHC class I, MHC class II, and cancer germline antigens in neuroblastoma

Cancer Immunology Immunotherapy ◽

10.1007/s00262-004-0603-z ◽

2004 ◽

Vol 54 (4) ◽

pp. 400-406 ◽

Cited By ~ 49

Author(s):

Matthias W�lfl ◽

Achim A. Jungbluth ◽

Federico Garrido ◽

Teresa Cabrera ◽

Sharon Meyen-Southard ◽

...

Keyword(s):

Mhc Class I ◽

Mhc Class Ii ◽

Class Ii ◽

Class I ◽

Class I Mhc ◽

Cancer Germline

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The Major Histocompatibility Complex of Old World Camels—A Synopsis

Cells ◽

10.3390/cells8101200 ◽

2019 ◽

Vol 8 (10) ◽

pp. 1200 ◽

Cited By ~ 1

Author(s):

Plasil ◽

Wijkmark ◽

Elbers ◽

Oppelt ◽

Burger ◽

...

Keyword(s):

Major Histocompatibility Complex ◽

Mhc Class I ◽

Mhc Class Ii ◽

Class Ii ◽

Class I ◽

Class Iii ◽

Old World ◽

Histocompatibility Complex ◽

Mhc Class Iii ◽

Antigen Presenting

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 and II genes encoding antigen presenting molecules. Based on this knowledge and using new camel genomic resources, we constructed an improved genomic map of the entire MHC region of Old World camels. The MHC class III sub-region shows a standard organization similar to that of pig or cattle. The overall genomic structure of the camel MHC is more similar to pig MHC than to cattle MHC. This conclusion is supported by differences in the organization of the MHC class II sub-region, absence of functional DY genes, different organization of MIC genes in the MHC class I sub-region, and generally closer evolutionary relationships of camel and porcine MHC gene sequences analyzed so far.

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Major Histocompatibility Complex Class II and Programmed Death Ligand 1 Expression Predict Outcome After Programmed Death 1 Blockade in Classic Hodgkin Lymphoma

Journal of Clinical Oncology ◽

10.1200/jco.2017.77.3994 ◽

2018 ◽

Vol 36 (10) ◽

pp. 942-950 ◽

Cited By ~ 106

Author(s):

Margaretha G.M. Roemer ◽

Robert A. Redd ◽

Fathima Zumla Cader ◽

Christine J. Pak ◽

Sara Abdelrahman ◽

...

Keyword(s):

Mhc Class I ◽

Mhc Class Ii ◽

Class Ii ◽

Class I ◽

Histocompatibility Complex ◽

Classic Hodgkin Lymphoma ◽

Programmed Death ◽

Clinical Responses ◽

Programmed Death 1 ◽

Cell Expression

Purpose Hodgkin Reed-Sternberg (HRS) cells evade antitumor immunity by multiple means, including gains of 9p24.1/ CD274(PD-L1)/ PDCD1LG2(PD-L2) and perturbed antigen presentation. Programmed death 1 (PD-1) receptor blockade is active in classic Hodgkin lymphoma (cHL) despite reported deficiencies of major histocompatibility complex (MHC) class I expression on HRS cells. Herein, we assess bases of sensitivity to PD-1 blockade in patients with relapsed/refractory cHL who were treated with nivolumab (anti–PD-1) in the CheckMate 205 trial. Methods HRS cells from archival tumor biopsies were evaluated for 9p24.1 alterations by fluorescence in situ hybridization and for expression of PD ligand 1 (PD-L1) and the antigen presentation pathway components—β2-microglobulin, MHC class I, and MHC class II—by immunohistochemistry. These parameters were correlated with clinical responses and progression-free survival (PFS) after PD-1 blockade. Results Patients with higher-level 9p24.1 copy gain and increased PD-L1 expression on HRS cells had superior PFS. HRS cell expression of β2-microglobulin/MHC class I was not predictive for complete remission or PFS after nivolumab therapy. In contrast, HRS cell expression of MHC class II was predictive for complete remission. In patients with a > 12-month interval between myeloablative autologous stem-cell transplantation and nivolumab therapy, HRS cell expression of MHC class II was associated with prolonged PFS. Conclusion Genetically driven PD-L1 expression and MHC class II positivity on HRS cells are potential predictors of favorable outcome after PD-1 blockade. In cHL, clinical responses to nivolumab were not dependent on HRS cell expression of MHC class I.

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Nicotinamide decreases MHC class II but not MHC class I expression and increases intercellular adhesion molecule-1 structures in non-obese diabetic mouse pancreas

Journal of Endocrinology ◽

10.1677/joe.0.1600389 ◽

1999 ◽

Vol 160 (3) ◽

pp. 389-400 ◽

Cited By ~ 8

Author(s):

G Papaccio ◽

E Ammendola ◽

FA Pisanti

Keyword(s):

Mhc Class I ◽

Mhc Class Ii ◽

Adhesion Molecule ◽

Nod Mice ◽

Class Ii ◽

Intercellular Adhesion ◽

Class I ◽

Intercellular Adhesion Molecule ◽

Nitrite Accumulation ◽

Intercellular Adhesion Molecule 1

Pancreases of untreated and nicotinamide (NIC)-treated pre-diabetic (10-week-old) and overtly diabetic (25-week-old) female NOD (non-obese diabetic) mice and of NON (non-obese non-diabetic) control mice were studied, with the following results. (1) Islets and ducts of overtly diabetic untreated NOD mice (25-week-old) were found to express low levels of MHC class I and II molecules, like NON controls, and high levels of adhesive molecules. (2) NIC was able to slightly affect glycaemia and insulitis, slowing down diabetes progression. Moreover it significantly decreased MHC class II expression (but not class I) in vivo by week 10, and significantly enhanced intercellular adhesion molecule-1 (ICAM-1) expression, mainly by week 25, within the pancreas, where 5-bromo-2'-deoxyuridine positive nuclei and insulin positive cells were present, demonstrating that a stimulation of endocrine cell proliferation occurs. (3) In addition, NIC partly counteracted the fall of superoxide dismutase levels, observed in untreated diabetic NOD animals. (4) In vitro studies demonstrated that NIC: (i) was able to significantly reduce nitrite accumulation and to increase NAD+NADH content significantly, and (ii) was able to increase the levels of interleukin-4, a T helper 2 lymphocyte (Th2) protective cytokine, and of interferon-alpha (IFN-alpha), which is known to be able to induce MHC class I and ICAM-1 but not MHC class II expression, as well as IFN-gamma, which is also known to be able to induce MHC class I and ICAM-1 expression. The latter, although known to be a proinflammatory Th1 cytokine, has also recently been found to exert an anti-diabetogenic role. This study therefore clearly shows that adhesive mechanisms are ongoing during the later periods of diabetes in pancreatic ducts of NOD mice, and suggests they may be involved in a persistence of the immune mechanisms of recognition, adhesion and cytolysis and/or endocrine regeneration or differentiation processes, as both NIC-increased ICAM-1 expression and 5-bromo-2'-deoxyuridine positivity imply. The effects of NIC on MHC class II (i.e. a reduction) but not class I, and, mainly, on ICAM-1 expression (i.e. an increase), together with the increase in Th2 protective cytokine levels are very interesting, and could help to explain its mechanism of action and the reasons for alternate success or failure in protecting against type 1 diabetes development.

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