Virus Evasion of MHC Class I Molecule Presentation

Petersen, Jason L.; Morris, Chantey R.; Solheim, Joyce C.

doi:10.4049/jimmunol.171.9.4473

Cited by 88 publications

(59 citation statements)

References 101 publications

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“…Viruses have developed numerous strategies to evade HLA-mediated immune detection, including mechanisms that directly interfere with the presentation of viral epitopes and HLA molecules on the cell surface 42,43,44 . For example, HIV-1 can increase cellular endocytosis of HLA molecules via nef 45,46 , limit HLA transcription and peptide processing via tat 47,48 and suppress TAP-mediated peptide transport into the endoplasmic reticulum 49 .…”

Section: Discussionmentioning

confidence: 99%

MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape

Pymm

Illing

Ramarathinam

et al. 2017

Nat Struct Mol Biol

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Section: Discussionmentioning

confidence: 99%

MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape

Pymm

Illing

Ramarathinam

et al. 2017

Nat Struct Mol Biol

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“…Many viruses have developed diverse strategies to disrupt specifically the expression of these complexes. 64,[143][144][145][146] A number of virus-encoded gene products, the VIPRs, have been found to interfere with the MHC class I antigen expression. Distinct molecular mechanisms have been found to cause total HLA class I antigen loss, HLA class I downregulation or selective HLA class I allospecificity loss or downregulation in virus-infected cells.…”

Section: Resultsmentioning

confidence: 99%

Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation

Seliger

Ritz

Ferrone

2005

Intl Journal of Cancer

113

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In humans as in other animal species, CD81 cytotoxic T lymphocytes (CTLs) play an important if not the major role in controlling virus-infected and malignant cell growth. The interactions between CD81 T cells and target cells are mediated by human leukocyte antigen (HLA) class I antigens loaded with viral and tumor antigen-derived peptides along with costimulatory receptor/ligand stimuli. Thus, to escape from CD8 1 T-cell recognition and destruction, viruses and tumor cells have developed strategies to inhibit the expression and/or function of HLA class I antigens. In contrast, cells with downregulated MHC class I surface expression can be recognized by NK cells, although NK cell-mediated lysis could be abrogated by the expression of inhibiting NK cell receptors. This review discusses the molecular mechanisms utilized by viruses to inhibit the formation, transport and/or expression of HLA class I antigen/peptide complexes on the cell surface. The knowledge about viral interference with MHC class I antigen presentation is not only crucial to understand the pathogenesis of viral diseases, but contributes also to the design of novel strategies to counteract the escape mechanisms utilized by viruses. These investigations may eventually lead to the development of effective immunotherapies to control viral infections and virus-associated malignant diseases. ' 2005 Wiley-Liss, Inc.

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“…Potential explanations for this may be viral immune evasion and inefficient lymphocyte priming. CMV can evade MHC class I host responses by expressing several proteins (HCMV: US2, US3, US6, US8, US10, US11, and UL18; and MCMV: gp34, gp40, and gp48) (46). Although these proteins interfere with MHC class I binding, when they are removed, as from mutant viruses, CD8…”

Section: Discussionmentioning

confidence: 99%

CD4⁺T-Cell Reconstitution Reduces Cytomegalovirus in the Immunocompromised Brain

Reuter¹,

Wilson²,

Idoko³

et al. 2005

J Virol

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Cytomegalovirus (CMV) infection is the most common opportunistic infection of the central nervous systemin patients with human immunodeficiency virus or AIDS or on immunosuppressive drug therapy. Despite medical management, infection may be refractory to treatment and continues to cause significant morbidity and mortality. We investigated adoptive transfer as an approach to treat and prevent neurotropic CMV infection in an adult immunodeficient mouse model. SCID mice were challenged with intracranial murine CMV (MCMV) and reconstituted with MCMV-or vesicular stomatitis virus (VSV)-sensitized splenocytes, T cells, or T-cell subsets. T cells labeled with vital dye or that constitutively generated green fluorescent protein (GFP) were identified in the brain as early as 3 days following peripheral transfer. Regardless of specificity, activated T cells localized to regions of the brain containing CMV, however, only those specific for CMV were effective at clearing virus. Reconstitution with unsorted MCMV-immune splenocytes, enriched T-cell fractions, or CD4؉ cells significantly reduced virus levels in the brain within 7 days and also prevented clinical disease, in significant contrast with mice given VSV-immune unsorted splenocytes, MCMV-immune CD8 ؉ T cells, and SCID control mice. Results suggest CMV-immune T cells (particularly CD4 ؉ ) rapidly cross the blood-brain barrier, congregate at sites of specific CMV infection, and functionally eliminate acute CMV within the brain. In addition, when CMV-immune splenocytes were administered prior to a peripheral CMV challenge, CMV entry into the immunocompromised brain was prevented. Systemic adoptive transfer may be a rapid and effective approach to preventing CMV entrance into the brain and for reducing neurotropic infection.

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Virus Evasion of MHC Class I Molecule Presentation

Cited by 88 publications

References 101 publications

MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape

MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape

Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation

CD4⁺T-Cell Reconstitution Reduces Cytomegalovirus in the Immunocompromised Brain

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Virus Evasion of MHC Class I Molecule Presentation

Cited by 88 publications

References 101 publications

MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape

MHC-I peptides get out of the groove and enable a novel mechanism of HIV-1 escape

Molecular mechanisms of HLA class I antigen abnormalities following viral infection and transformation

CD4+T-Cell Reconstitution Reduces Cytomegalovirus in the Immunocompromised Brain

Contact Info

Product

Resources

About

CD4⁺T-Cell Reconstitution Reduces Cytomegalovirus in the Immunocompromised Brain