Naslov
Immune Evasion of T Cell and NK response by Cytomegalovirus Proteins

Autori
Jonjić, Stipan

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
1. slovenski imunološki kongres z mednarodno udeležbo / Kotnik, Vladimir - Ljubljana : Medicinski razgledi, 2000, 148-149

Skup
1. slovenski imunološki kpongres z mednarodno udeležbo

Mjesto i datum
Portorož, Slovenija, 2000

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
cytomegalovirus-immunology; NK cells; T lymphocytes; CD8 positive T lymphocytes

Sažetak
Cytomegaloviruses (CMVs) are kept under tight immune control in immunocompetent hosts but establish latent infections and, after periodic reactivation from latency, use a panel of immune evasion proteins to survive and replicate in the face of fully primed host immunity. Acute infections or reactivation of latent virus in immunosuppressed host, however, can result in serious disease and mortality. AIDS patients, as well as solid organ and bone marrow transplant recipients, are particularly vulnerable to multi-organ disease due to human cytomegalovirus (HCMV) infection. The CD8+ T cells are decisive for control of infections by CMVs in immunocompetent hosts. To achieve effective surveillance of virus-infected cells, CD8’+ T cells need to recognize viral peptides in the context of MHC class I molecules at the surface of infected cells. Presentation of viral peptides via this pathway requires degradation of viral proteins by the proteasomes and the translocation of the peptides into the endoplasmic reticulum (ER) by transporters associated with antigen presentation (TAP) for loading into the binding groove of nascent MHC class I molecules and the subsequent egress of MHC complexes to the cell surface. The HCMV encodes several polypeptides which can independently interfere with MHC class I antigen presentation to inhibit efficient recognition of infected cells by CD8+ CTL. In mouse CMV (MCMV) at least three genes affect MHC class I molecules. The MCMV early glycoprotein gp40 encoded by the m152 gene blocks the export of MHC class I complexes from the ER-Golgi intermediate compartment (ERGIC) and cis-Golgi and thereby prevents the presentation of viral peptides to CTL. Two additional MCMV proteins, the products of the m04 and of the m06 genes, form complexes with MHC class I molecules. Since the downregulation of surface MHC class I by viral immune evasion proteins should make the infected cells susceptible to attack by NK cells that recognize the “missing self”, the counterstrategies of CMVs to evade NK cell control are needed. In addition to interference with the MHC class I antigen presentation pathway, recent data also indicate that the MHC class II pathway of antigen presentation to CD4+ T cells can be a target for immune evasion genes of HCMV. The potential significance of immune evasion genes of HCMV and MCMV for viral pathogenesis and virus control in vivo will be discussed.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

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