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Transplantation ; 69(4): 687-90, 2000 Feb 27.
Article in English | MEDLINE | ID: mdl-10708135

ABSTRACT

Interferon-gamma stimulates major histocompatibility complex (MHC) class I antigen processing and presentation by inducing the expression of major histocompatibility complex class I heavy chains, beta2-microglobulin, the transporter associated with antigen processing, and components of the proteasome complex. We demonstrate that this effect of interferon-gamma on the major histocompatibility complex class I pathway is inhibited in human cytomegalovirus-infected fibroblasts and endothelial cells. This is the result of a direct human cytomegalovirus/cell interaction leading to a block in interferon-gamma signal transduction beginning at early times after infection and peaking at 72 hr after infection. These observations suggest a novel level of herpesvirus interference with antigen processing: protection of infected cells from the immunoregulatory effects of interferon-gamma. Thus protected, human cytomegalovirus persists and may exacerbate graft rejection or lead to fulminant infection in the immunocompromised transplant recipient.


Subject(s)
Cytomegalovirus Infections/physiopathology , Histocompatibility Antigens Class I/physiology , Interferon-gamma/antagonists & inhibitors , Interferon-gamma/pharmacology , Antigen Presentation/drug effects , Antigen Presentation/physiology , Electrophoresis , Epithelial Cells/immunology , Epithelial Cells/metabolism , Epithelial Cells/virology , Fibroblasts/immunology , Fibroblasts/metabolism , Fibroblasts/virology , Gene Expression , Histocompatibility Antigens Class I/immunology , Humans , Interferon-gamma/genetics , Kinetics , Signal Transduction/drug effects , Up-Regulation/drug effects
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