Cytomegalovirus and transcriptional down-regulation of major histocompatibility complex class II expression.
CD4(+)T lymphocytes are a significant component of the afferent and efferent arms of adaptive immunity and are critical for controlling viral infections. CD4(+)T lymphocytes secrete cytokines that augment CD8(+)T lymphocyte and B lymphocyte responses and directly inhibit viral replication. The interface between the CD4(+)T lymphocyte and virus is the major histocompatibility complex (MHC) class II molecule. Cytomegalovirus, a beta-herpesvirus, has evolved mechanisms for inhibiting MHC class II expression and thus escaping CD4(+)T lymphocyte immunosurveillance. Herein, we review cytomegalovirus-mediated down-regulation of inducible and constitutive MHC class II expression, while focusing on lesions that occur at the level of MHC class II transcription.
Miller
D M
DM
Department of Pathology, The Ohio State University College of Medicine and Public Health, Columbus, OH 43210, USA.
Cebulla
C M
CM
Rahill
B M
BM
Sedmak
D D
DD
D000818:Animals; D003587:Cytomegalovirus / Q000276:immunology* / Q000472:pathogenicity; D003586:Cytomegalovirus Infections / Q000235:genetics* / Q000276:immunology* / Q000821:virology; D015536:Down-Regulation / Q000235:genetics* / Q000276:immunology*; D005802:Genes, MHC Class II / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis* / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D014158:Transcription, Genetic / Q000276:immunology*
D000949:Histocompatibility Antigens Class II