scholarly journals Evidence for the Influence of the Iron Regulatory MHC Class I Molecule HFE on Tumor Progression in Experimental Models and Clinical Populations

2014 ◽  
Vol 6 ◽  
pp. 1-12 ◽  
Author(s):  
Cody Weston and James Connor
Keyword(s):  
Tumor Progression ◽  
Mhc Class I ◽  
Experimental Models ◽  
Class I ◽  
Mhc Class I Molecule ◽  
Clinical Populations

scholarly journals Major histocompatibility complex class I molecules mediate association of SV40 with caveolae.

1997 ◽  
Vol 8 (1) ◽  
pp. 47-57 ◽  
Author(s):  
E Stang ◽  
J Kartenbeck ◽  
R G Parton
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
Mammalian Cells ◽  
Simian Virus 40 ◽  
Class I ◽  
Major Histocompatibility ◽  
Surface Binding ◽  
Histocompatibility Complex ◽  
Mhc Class I Molecule ◽  
Mhc Class I Molecules

Simian virus 40 (SV40) has been shown to enter mammalian cells via uncoated plasma membrane invaginations. Viral particles subsequently appear within the endoplasmic reticulum. In the present study, we have examined the surface binding and internalization of SV40 by immunoelectron microscopy. We show that SV40 associates with surface pits which have the characteristics of caveolae and are labeled with antibodies to the caveolar marker protein, caveolin-1. SV40 is believed to use major histocompatibility complex (MHC) class I molecules as cell surface receptors. Using a number of MHC class I-specific monoclonal antibodies, we found that both viral infection and association of virus with caveolae were strongly reduced by preincubation with anti-MHC class I antibodies. Because binding of SV40 to MHC class I molecules may induce clustering, we investigated whether antibody cross-linked class I molecules also redistributed to caveolae. Clusters of MHC class I molecules were indeed shown to be specifically associated with caveolin-labeled surface pits. Taken together, the results suggest that SV40 may make use of MHC class I molecule clustering and the caveolae pathway to enter mammalian cells.

scholarly journals Discovery of an ancient MHC category with both class I and class II features

2021 ◽  
Vol 118 (51) ◽  
pp. e2108104118
Author(s):  
Kazuhiko Okamura ◽  
Johannes M. Dijkstra ◽  
Kentaro Tsukamoto ◽  
Unni Grimholt ◽  
Geert F. Wiegertjes ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Class Ii ◽  
Class I ◽  
Sequence Motifs ◽  
Critical Question ◽  
Specific Sequence ◽  
Mhc Molecules ◽  
Mhc Class I Molecule ◽  
Chain Organization ◽  
Lymphocyte Populations

Two classes of major histocompatibility complex (MHC) molecules, MHC class I and class II, play important roles in our immune system, presenting antigens to functionally distinct T lymphocyte populations. However, the origin of this essential MHC class divergence is poorly understood. Here, we discovered a category of MHC molecules (W-category) in the most primitive jawed vertebrates, cartilaginous fish, and also in bony fish and tetrapods. W-category, surprisingly, possesses class II–type α- and β-chain organization together with class I–specific sequence motifs for interdomain binding, and the W-category α2 domain shows unprecedented, phylogenetic similarity with β2-microglobulin of class I. Based on the results, we propose a model in which the ancestral MHC class I molecule evolved from class II–type W-category. The discovery of the ancient MHC group, W-category, sheds a light on the long-standing critical question of the MHC class divergence and suggests that class II type came first.

scholarly journals A Specialist Macaque MHC Class I Molecule with HLA-B*27–like Peptide-Binding Characteristics

2017 ◽  
Vol 199 (10) ◽  
pp. 3679-3690 ◽  
Author(s):  
Natasja G. de Groot ◽  
Corrine M. C. Heijmans ◽  
Arnoud H. de Ru ◽  
George M. C. Janssen ◽  
Jan W. Drijfhout ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Peptide Binding ◽  
Class I ◽  
Binding Characteristics ◽  
Mhc Class I Molecule

scholarly journals T Cell Recognition of an Engineered MHC Class I Molecule: Implications for Peptide-Independent Alloreactivity

2002 ◽  
Vol 169 (4) ◽  
pp. 1887-1892 ◽  
Author(s):  
Vladimir Janković ◽  
Kristin Remus ◽  
Alberto Molano ◽  
Janko Nikolich-Žugich
Keyword(s):  
T Cell ◽  
Mhc Class I ◽  
Class I ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Mhc Class I Molecule

Design of Analogs of Trapoxin, Cyl-1, and Chlamydocin for MHC Class-I Molecule Up-Regulation

2001 ◽  
pp. 528-529
Author(s):  
Norikazu Nishino ◽  
Tamaki Kato ◽  
Yasuhiko Komatsu ◽  
Minora Yoshida
Keyword(s):  
Mhc Class I ◽  
Class I ◽  
Mhc Class I Molecule

scholarly journals Effect of a tapasin mutant on the assembly of the mouse MHC class I molecule H2‐K d

2009 ◽  
Vol 88 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Laura C Simone ◽  
Xiaojian Wang ◽  
Amit Tuli ◽  
Joyce C Solheim
Keyword(s):  
Mhc Class I ◽  
Class I ◽  
Mhc Class I Molecule

scholarly journals MHC class I–deficient natural killer cells acquire a licensed phenotype after transfer into an MHC class I–sufficient environment

2010 ◽  
Vol 207 (10) ◽  
pp. 2073-2079 ◽  
Author(s):  
Julie M. Elliott ◽  
Joseph A. Wahle ◽  
Wayne M. Yokoyama
Keyword(s):  
Bone Marrow ◽  
Nk Cells ◽  
Natural Killer ◽  
Mhc Class I ◽  
Interferon Γ ◽  
Class I ◽  
Target Cells ◽  
Major Histocompatability Complex ◽  
Gain Of Function ◽  
Mhc Class I Molecule

In MHC class I–deficient hosts, natural killer (NK) cells are hyporesponsive to cross-linking of activation receptors. Functional competence requires engagement of a self–major histocompatability complex (MHC) class I–specific inhibitory receptor, a process referred to as “licensing.” We previously suggested that licensing is developmentally determined in the bone marrow. In this study, we find that unlicensed mature MHC class I–deficient splenic NK cells show gain-of-function and acquire a licensed phenotype after adoptive transfer into wild-type (WT) hosts. Transferred NK cells produce WT levels of interferon-γ after engagement of multiple activation receptors, and degranulate at levels equivalent to WT NK cells upon coincubation with target cells. Only NK cells expressing an inhibitory Ly49 receptor specific for a cognate host MHC class I molecule show this gain-of-function. Therefore, these findings, which may be relevant to clinical bone marrow transplantation, suggest that neither exposure to MHC class I ligands during NK development in the BM nor endogenous MHC class I expression by NK cells themselves is absolutely required for licensing.

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