scholarly journals Immune response in human melanoma after transfer of an allogeneic class I major histocompatibility complex gene with DNA-liposome complexes

1996 ◽  
Vol 93 (26) ◽  
pp. 15388-15393 ◽  
Author(s):  
G. J. Nabel ◽  
D. Gordon ◽  
D. K. Bishop ◽  
B. J. Nickoloff ◽  
Z.-y. Yang ◽  
...  
Keyword(s):  
Immune Response ◽  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Gene ◽  
Human Melanoma ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

scholarly journals Downregulation of major histocompatibility complex class I in bovine papillomas

2004 ◽  
Vol 85 (10) ◽  
pp. 2809-2814 ◽  
Author(s):  
E. H. Araibi ◽  
B. Marchetti ◽  
G. H. Ashrafi ◽  
M. S. Campo
Keyword(s):  
Immune Response ◽  
Major Histocompatibility Complex ◽  
Immune System ◽  
Major Histocompatibility Complex Class ◽  
Class I ◽  
Host Immune System ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Mhc I ◽  
Histocompatibility Complex

Bovine papillomavirus (BPV) induces papillomas in cattle; in the great majority of cases, these regress due to the host immune response, but they can persist and progress to malignancy. Even in the absence of malignant transformation, BPV infection persists for a significant period of time before activation of the host immune system, suggesting that the host immune system is unaware of, or disabled by, BPV. E5 is the major oncoprotein of BPV, which, in addition to its transforming properties, downregulates the expression and transport to the cell surface of major histocompatibility complex class I (MHC I). Here, it is shown that co-expression of MHC I and E5 in papillomas caused by BPV-4 infection is mutually exclusive, in agreement with the inhibition of surface MHC I expression by E5 that is observed in vitro. The inhibition of MHC expression in E5-expressing papilloma cells could explain the long period that is required for activation of the immune response and has implications for the progression of papillomas to the malignant stage; absence of peptide presentation by MHC I to cytotoxic T lymphocytes would allow the infected cells to evade the host cellular immune response and allow the lesions to persist.

Expression of a microinjected porcine class I major histocompatibility complex gene in transgenic mice

Science ◽  
1985 ◽  
Vol 228 (4699) ◽  
pp. 577-580 ◽  
Author(s):  
W. Frels ◽  
J. Bluestone ◽  
R. Hodes ◽  
M. Capecchi ◽  
D. Singer
Keyword(s):  
Major Histocompatibility Complex ◽  
Transgenic Mice ◽  
Major Histocompatibility Complex Gene ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

scholarly journals Downregulation of Major Histocompatibility Complex Class I Molecules by Kaposi's Sarcoma-Associated Herpesvirus K3 and K5 Proteins

2000 ◽  
Vol 74 (11) ◽  
pp. 5300-5309 ◽  
Author(s):  
Satoshi Ishido ◽  
Chunyang Wang ◽  
Bok-Soo Lee ◽  
George B. Cohen ◽  
J. U. Jung
Keyword(s):  
Immune Response ◽  
Major Histocompatibility Complex ◽  
Amino Acid ◽  
Mhc Class I ◽  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Mhc Class I Molecules

ABSTRACT The T-cell-mediated immune response plays a central role in the defense against intracellular pathogens. To avoid this immune response, viruses have evolved elaborate mechanisms that target and modulate many different aspects of the host's immune system. A target common to many of these viruses is the major histocompatibility complex (MHC) class I molecules. Kaposi's sarcoma-associated herpesvirus (KSHV) encodes K3 and K5 zinc finger membrane proteins which remove MHC class I molecules from the cell surface. K3 and K5 exhibit 40% amino acid identity to each other and localize primarily near the plasma membrane. While K3 and K5 dramatically downregulated class I molecules, they displayed different specificities in downregulation of HLA allotypes. K5 significantly downregulated HLA-A and -B and downregulated HLA-C only weakly, but not HLA-E, whereas K3 downregulated all four HLA allotypes. This selective downregulation of HLA allotypes by K5 was partly due to differences in amino acid sequences in their transmembrane regions. Biochemical analyses demonstrated that while K3 and K5 did not affect expression and intracellular transport of class I molecules, their expression induced rapid endocytosis of the molecules. These results demonstrate that KSHV has evolved a novel immune evasion mechanism by harboring similar but distinct genes, K3 and K5, which target MHC class I molecules in different ways.

Sign in / Sign up

Export Citation Format

Share Document