How Dna Viruses Perturb Functional Mhc Expression To Alter Immune Recognition

McFadden, Grant; Kane, Kevin P.

doi:10.1016/s0065-230x(08)60400-5

Cited by 66 publications

(25 citation statements)

References 533 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Using HLA-2.1 transgenic mice four immunogenic peptides were identified in vivo [E6 (29)(30)(31)(32)(33)(34)(35)(36)(37)(38), E7 (11)(12)(13)(14)(15)(16)(17)(18)(19)(20), E7 (82)(83)(84)(85)(86)(87)(88)(89)(90), and E7 (86-93)]. In addition, CTL induction of PBMC from humans confirmed immunogenicity, in vitro, of three of the four peptides [E7 (11)(12)(13)(14)(15)(16)(17)(18)(19)(20), E7 (82)(83)(84)(85)(86)(87)(88)(89)(90), and E7 (86-93)]. CTL to one of the...…”

Section: Adaptive Cell-mediated Immunitymentioning

confidence: 99%

“…They concluded that HPV may evade immunological recognition by downregulating TAP-1. Others have cautioned, however, that MHC class I downregulation may be the result of altered levels of or sensitivity to cytokines, such as IFN-␥ and TNF, rather than direct effects of viral infection (88). Regardless of the underlying reasons for changes in MHC class I expression, the data suggest that in persistent HPV infection or HPV-associated malignancy, loss or downregulation of MHC class I expression may contribute significantly to diminished recognition and removal of infected cells by CTL.…”

Section: Adaptive Cell-mediated Immunitymentioning

confidence: 99%

See 1 more Smart Citation

Cell-Mediated Immune Response to Human Papillomavirus Infection

Scott

Nakagawa

Moscicki

2001

Clin Diagn Lab Immunol

234

217

View full text Add to dashboard Cite

Acquisition of human papillomavirus (HPV) results in an infection of variable duration which may or may not be associated with clinically apparent lesions. Lesions caused by skintropic HPV types generally manifest as cutaneous warts and most often resolve over a period of months to years. On the other hand, anogenital infections are more likely to remain clinically inapparent. The development of DNA amplificationbased tests has demonstrated that anogenital infections are quite common and generally self-limited. For example, we and others have shown by PCR testing of multiple samples collected at different points in time-that 70 to 90% of sexually active adolescents and young women who develop an incident cervical HPV infection will show clearance of infection within 12 to 30 months (47,61,94). The factors influencing the natural history of these infections are not well understood. Given that persistent anogenital infection with oncogenic HPV types is associated with increased risk of neoplasia and invasive cancers (22,59,70,71,94,124) and that cervical carcinoma remains a leading cause of death among women in developing countries (129), understanding these factors is of considerable importance.Substantial effort has been directed recently at understanding the role of the host's immune response in the natural history of HPV, and in particular, anti-viral, cell-mediated immunity. Empirical evidence for the importance of cell-mediated immunity in control of HPV infection comes from an extensive body of literature documenting the increased prevalence of HPV infection and associated disease among immunosuppressed populations, including those with iatrogenic immunosuppression such as renal transplant recipients and individuals with human immunodeficiency virus (HIV) infection. Sillman and coauthors (128) reported in 1984 on 20 immunosuppressed women with various causes of immunosuppression who had lower genital neoplasia, describing evidence of associated HPV infection in all 20. Penn, in 1986, reported a 100-fold increase in cancer of the vulva and anus in renal transplant recipients (111). In the 1990s, as molecular testing for HPV infection came into its own, several reports confirmed increased incidence of HPV infection (50) and associated morbidities, including warts (77) and cervical squamous intraepithelial lesions (SIL) (104), among immunosuppressed renal transplant recipients.The most persuasive evidence for the association between cellular immune defects and HPV infection and related morbidities comes from persons with HIV infection. Such individuals show increased prevalence of anogenital HPV infection (31, 32, 60, 105-107) as well as longer periods of HPV persistence (31,40,46,90,136). In addition, infection with multiple HPV types and with oncogenic types are more common (9,31,46,78,90,107,136). Associations between markers of HIV disease status (e.g., viral load and CD4 lymphocyte count) and HPV infection have been inconsistent. Most studies have suggested that advanced disease and greater immunological ...

show abstract

Section: Adaptive Cell-mediated Immunitymentioning

confidence: 99%

Section: Adaptive Cell-mediated Immunitymentioning

confidence: 99%

Cell-Mediated Immune Response to Human Papillomavirus Infection

Scott

Nakagawa

Moscicki

2001

Clin Diagn Lab Immunol

234

217

View full text Add to dashboard Cite

show abstract

“…Their recognition occurs through the interaction between the T-cell receptor of a cytotoxic cell and a viral peptide bound to a class I major histocompatibility complex (MHC-I) molecule (31). Several mechanisms for interfering with MHC-I cell surface display have been developed by large DNA viruses (28). Basically, all the steps of the trafficking of MHC-I molecules and their association with peptides are targets of viral strategies: these can be the inhibition of transporter associated with antigen processing (TAP)-dependent peptide translocation from the cytoplasm to the endoplasmic reticulum (ER) (24); the accumulation of MHC-I in the ER, preventing the accession of assembled molecules to the cell surface (2); or the translocation of ER-resident MHC-I molecules to the cytosol and their subsequent degradation by proteasomes (46).…”

mentioning

confidence: 99%

Myxoma Virus Leukemia-Associated Protein Is Responsible for Major Histocompatibility Complex Class I and Fas-CD95 Down-Regulation and Defines Scrapins, a New Group of Surface Cellular Receptor Abductor Proteins

Guérin

Gelfi

Boullier

et al. 2002

J Virol

101

103

View full text Add to dashboard Cite

Down-modulation of major histocompatibility class I (MHC-I) molecules is a viral strategy for survival in the host. Myxoma virus, a member of the Poxviridae family responsible for rabbit myxomatosis, can downmodulate the expression of MHC-I molecules, but the viral factor(s) has not been described. We cloned and characterized a gene coding for an endoplasmic reticulum (ER)-resident protein containing an atypical zinc finger and two transmembrane domains, which we called myxoma virus leukemia-associated protein (MV-LAP). MV-LAP down-regulated surface MHC-I and Fas-CD95 molecules upon transfection; the mechanism probably involves an exacerbation of endocytosis and was lost when the ER retention signal was removed. In addition, the lytic activity of MHC-I-restricted antigen-specific cytolytic T lymphocytes (CTL) against myxoma virus-infected antigen-presenting target cells was significantly reduced, revealing a strong correlation between MHC-I down-regulation by MV-LAP and CTL killing in vitro. In vivo experiments with a knockout virus showed that MV-LAP is a virulence factor, potentially involved in the immunosuppression characteristic of myxomatosis. Data bank analysis revealed that MV-LAP has homologs in herpesviruses and other poxviruses.We propose the name "scrapins" to define a new group of ER-resident surface cellular receptor abductor proteins. The down-regulation of cell surface molecules by scrapins probably helps protect infected cells during viral infections.

show abstract

“…A target common to many of these viruses are the major histocompatibility complex (MHC) class I antigens (4,5). Class I products play a central role in recognition and subsequent lysis by cytotoxic T lymphocytes (6), a key component of the cellular arm of the human immune system.…”

mentioning

confidence: 99%

Human cytomegalovirus US3 impairs transport and maturation of major histocompatibility complex class I heavy chains.

Jones

Wiertz

Sun

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

376

321

View full text Add to dashboard Cite

The human cytomegalovirus (HCMV) early glycoprotein products of the US1l and US2 open reading frames cause increased turnover of major histocompatibility complex (MHC) class I heavy chains. Since US2 is homologous to another HCMV gene (US3), we hypothesized that the US3 gene product also may affect MHC class I expression. In cells constitutively expressing the HCMV US3 gene, MHC class I heavy chains formed a stable complex with 132-microglobulin. However, maturation of the N-linked glycan of MHC class I heavy chains was impaired in US3+ cells. The glycoprotein product of US3 (gpUS3) occurs mostly in a high-mannose form and coimmunoprecipitates with 132-microglobulin associated class I heavy chains. Mature class I molecules were detected at steady state on the surface ofUS3+ cells, as in control cells. Substantial perinuclear accumulation of heavy chains was observed in US3+ cells. The data suggest that gpUS3 impairs egress of MHC class I heavy chains from the endoplasmic reticulum.

show abstract

How Dna Viruses Perturb Functional Mhc Expression To Alter Immune Recognition

Cited by 66 publications

References 533 publications

Cell-Mediated Immune Response to Human Papillomavirus Infection

Cell-Mediated Immune Response to Human Papillomavirus Infection

Myxoma Virus Leukemia-Associated Protein Is Responsible for Major Histocompatibility Complex Class I and Fas-CD95 Down-Regulation and Defines Scrapins, a New Group of Surface Cellular Receptor Abductor Proteins

Human cytomegalovirus US3 impairs transport and maturation of major histocompatibility complex class I heavy chains.

Contact Info

Product

Resources

About