scholarly journals Murine retroviruses control class I major histocompatibility antigen gene expression via a trans effect at the transcriptional level.

1987 ◽  
Vol 7 (7) ◽  
pp. 2406-2415 ◽  
Author(s):  
L D Wilson ◽  
D C Flyer ◽  
D V Faller
Keyword(s):  
Gene Expression ◽  
Class I ◽  
Transcriptional Level ◽  
Immune Recognition ◽  
Mrna Levels ◽  
Major Histocompatibility ◽  
Class I Mhc ◽  
Mhc Genes ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Moloney murine leukemia virus (M-MuLV) and Moloney murine sarcoma virus (M-MSV) exert a regulatory effect on the class I genes of the murine major histocompatibility complex (MHC). We have previously shown that M-MuLV infection of mouse fibroblasts results in a substantial increase in cell surface expression of H-2K, H-2D, and H-2L proteins, whereas M-MSV, upon coinfection of the same cells, is apparently able to override the MuLV-induced increase in H-2 expression. As a result of this modulation, immune recognition of the infected cells is profoundly altered. Our efforts have been directed toward elucidating the molecular basis for this phenomenon. We report here that stimulation of interferon production as a result of infection with MuLV does not occur and, therefore, is not the cause of MuLV-induced enhancement of MHC expression. Control of H-2 class I and beta 2-microglobulin gene expression by M-MuLV, and probably by M-MSV, takes place at the transcriptional level as indicated by nuclear runoff studies and analysis of steady-state mRNA levels. Our demonstration that M-MuLV controls expression of widely separated endogenous cellular genes (those coding for H-2D, H-2K, H-2L, and beta 2-microglobulin), transfected class I MHC genes, and unintegrated chimeric genes consisting of fragments of class I MHC genes linked to sequences encoding a procaryotic enzyme, chloramphenicol acetyltransferase, suggests that M-MuLV exerts its effect in trans and not by proviral integration in the vicinity of the H-2 gene complex. Finally, we show that the sequences of at least one MHC gene, which are responsive to trans regulation by M-MuLV, lie within 1.2 kilobases upstream of the initiation codon for that gene.

Murine retroviruses control class I major histocompatibility antigen gene expression via a trans effect at the transcriptional level

1987 ◽  
Vol 7 (7) ◽  
pp. 2406-2415
Author(s):  
L D Wilson ◽  
D C Flyer ◽  
D V Faller
Keyword(s):  
Gene Expression ◽  
Class I ◽  
Transcriptional Level ◽  
Immune Recognition ◽  
Mrna Levels ◽  
Major Histocompatibility ◽  
Class I Mhc ◽  
Mhc Genes ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Moloney murine leukemia virus (M-MuLV) and Moloney murine sarcoma virus (M-MSV) exert a regulatory effect on the class I genes of the murine major histocompatibility complex (MHC). We have previously shown that M-MuLV infection of mouse fibroblasts results in a substantial increase in cell surface expression of H-2K, H-2D, and H-2L proteins, whereas M-MSV, upon coinfection of the same cells, is apparently able to override the MuLV-induced increase in H-2 expression. As a result of this modulation, immune recognition of the infected cells is profoundly altered. Our efforts have been directed toward elucidating the molecular basis for this phenomenon. We report here that stimulation of interferon production as a result of infection with MuLV does not occur and, therefore, is not the cause of MuLV-induced enhancement of MHC expression. Control of H-2 class I and beta 2-microglobulin gene expression by M-MuLV, and probably by M-MSV, takes place at the transcriptional level as indicated by nuclear runoff studies and analysis of steady-state mRNA levels. Our demonstration that M-MuLV controls expression of widely separated endogenous cellular genes (those coding for H-2D, H-2K, H-2L, and beta 2-microglobulin), transfected class I MHC genes, and unintegrated chimeric genes consisting of fragments of class I MHC genes linked to sequences encoding a procaryotic enzyme, chloramphenicol acetyltransferase, suggests that M-MuLV exerts its effect in trans and not by proviral integration in the vicinity of the H-2 gene complex. Finally, we show that the sequences of at least one MHC gene, which are responsive to trans regulation by M-MuLV, lie within 1.2 kilobases upstream of the initiation codon for that gene.

scholarly journals Efficient dissociation of the p88 chaperone from major histocompatibility complex class I molecules requires both beta 2-microglobulin and peptide.

1992 ◽  
Vol 175 (6) ◽  
pp. 1653-1661 ◽  
Author(s):  
E Degen ◽  
M F Cohen-Doyle ◽  
D B Williams
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Heavy Chain ◽  
Class I ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Heavy Chains ◽  
Histocompatibility Complex ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Previously, we showed that an 88-kD protein (p88) associates rapidly and quantitatively with newly synthesized murine major histocompatibility complex class I molecules within the endoplasmic reticulum (ER). This interaction is transient and dissociation of p88 appears to be rate limiting for transport of class I molecules from the ER to the Golgi apparatus. In this report, we examine the relationship between p88 interaction and assembly of the ternary complex of class I heavy chain beta 2-microglobulin (beta 2m), and peptide ligand. In both murine and human beta 2m-deficient cells, in which little or no transport of class I heavy chains is observed, p88 remained associated with intracellular heavy chains throughout their lifetime. In murine RMA-S cells, which are apparently defective in accumulating peptide ligands for class I within the ER, prolonged association of p88 with "empty" heavy chain-beta 2m heterodimers was also observed. However, p88 dissociated slowly in parallel with the slow rate of ER to Golgi transport of empty class I molecules in these cells. The close correlation between p88 association and impaired class I transport suggests that p88 functions to retain incompletely assembled class I molecules in the ER. We propose that conformational changes in class I heavy chains induced by the binding of both beta 2m and peptide are required for efficient p88 dissociation and subsequent class I transport.

scholarly journals Expression of m157, a Murine Cytomegalovirus-Encoded Putative Major Histocompatibility Class I (MHC-I)-Like Protein, Is Independent of Viral Regulation of Host MHC-I

2006 ◽  
Vol 80 (1) ◽  
pp. 545-550 ◽  
Author(s):  
Sandeep K. Tripathy ◽  
Hamish R. C. Smith ◽  
Erika A. Holroyd ◽  
Jeanette T. Pingel ◽  
Wayne M. Yokoyama
Keyword(s):  
Antigen Processing ◽  
Cell Activation ◽  
Nk Cell ◽  
Class I ◽  
Murine Cytomegalovirus ◽  
Viral Gene ◽  
Major Histocompatibility ◽  
Class I Mhc ◽  
Mhc I ◽  
Beta 2 Microglobulin

ABSTRACT A murine cytomegalovirus (MCMV)-encoded protein, m157, has a putative major histocompatibility complex class I (MHC-I) structure and is recognized by the Ly49H NK cell activation receptor. Using a monoclonal antibody against m157, in this study we directly demonstrated that m157 is a cell surface-expressed glycophosphatidylinositol-anchored protein with early viral gene kinetics. Beta-2 microglobulin and TAP1 (transporter associated with antigen processing 1) were not required for its expression. MCMV-encoded proteins that down-regulate MHC-I did not affect the expression of m157. Thus, m157 is expressed on infected cells in a manner independent of viral regulation of host MHC-I.

scholarly journals Interleukin 10 up-regulates elastin gene expression in vivo and in vitro at the transcriptional level

1994 ◽  
Vol 302 (2) ◽  
pp. 331-333 ◽  
Author(s):  
S Reitamo ◽  
A Remitz ◽  
K Tamai ◽  
I Ledo ◽  
J Uitto
Keyword(s):  
Gene Expression ◽  
Interleukin 10 ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
Tgf Beta ◽  
Cultured Fibroblasts ◽  
Beta 2 ◽  
Elastin Gene

In immune cells, such as T cells and monocytes, interleukin 10 (IL-10) has regulatory functions on a number of cytokines, including IL-1, IL-2, IL-8 and tumour necrosis factor-alpha expression. However, the effects of IL-10 have not previously been studied in detail in connective-tissue cells. In the present study, we show that recombinant human IL-10 at physiological concentrations has direct effects on the expression of the human elastin gene both in vivo and in vitro. Transgenic mice expressing a human elastin promoter/chloramphenicol acetyltransferase (CAT) reporter gene construct were injected subcutaneously with IL-10 (1-100 ng) and the site of injection was biopsied after 24 h. CAT assay revealed an increase of up to 3.5-fold in the promoter activity with 10 ng of IL-10. Transforming growth factor-beta 2 (TGF-beta 2) is known to up-regulate elastin gene expression in cultured fibroblasts. When IL-10 was added to such cultures, the effects of TGF-beta 2 on elastin mRNA levels were synergistically potentiated. These results suggest that IL-10 has an up-regulatory effect on elastin gene expression.

The Interaction between Beta 2-Microglobulin (ssm) and Purified Class-I Major Histocompatibility (MHC) Antigen

1994 ◽  
Vol 39 (1) ◽  
pp. 64-72 ◽  
Author(s):  
L. O. PEDERSEN ◽  
A. S. HANSEN ◽  
A. C. OLSEN ◽  
J. GERWIEN ◽  
M. H. NISSEN ◽  
...  
Keyword(s):  
Class I ◽  
Major Histocompatibility ◽  
Beta 2 ◽  
Beta 2 Microglobulin ◽  
Mhc Antigen
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