Human Immunodeficiency Virus Type 1 Vpu Protein Interacts with CD74 and Modulates Major Histocompatibility Complex Class II Presentation

Hussain, Amjad; Wesley, Clement; Khalid, Mohammad; Chaudhry, Ashutosh; Jameel, Shahid

doi:10.1128/jvi.01373-07

Cited by 52 publications

(35 citation statements)

References 55 publications

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“…The recognition of Env, Pol, and Vpu antigens, but not Gag or Nef, by the NK cell-mediated ADCC response is curious. Surface expression of Env is clearly well described, and there is increasing evidence that the Vpu associates with the cell membrane and with MHC-II molecules, as recently reported (12). Interesting cell trafficking and surface expression of HIV proteins and vaccine targets may be revealed by further study of ADCC responses using this technology.…”

Section: Discussionmentioning

confidence: 84%

Robust NK Cell-Mediated Human Immunodeficiency Virus (HIV)-Specific Antibody-Dependent Responses in HIV-Infected Subjects

Stratov

Chung

Kent

2008

J Virol

108

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Antibody-dependent cellular cytotoxicity (ADCC) is a potentially effective adaptive immune response to human immunodeficiency virus (HIV) infection. The study of ADCC responses has been hampered by the lack of simple methods to quantify these responses and map effective epitopes. We serendipitously observed that standard intracellular cytokine assays on fresh whole blood from a cohort of 26 HIV-infected subjects identified non-T lymphocytes expressing gamma interferon (IFN-␥) in response to overlapping linear peptides spanning HIV-1 proteins. The effector cells were CD3

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Section: Discussionmentioning

confidence: 84%

Robust NK Cell-Mediated Human Immunodeficiency Virus (HIV)-Specific Antibody-Dependent Responses in HIV-Infected Subjects

Stratov

Chung

Kent

2008

J Virol

108

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“…1B). The modest residual reduction in surface MHCII levels in the cells infected with Nefdeficient HIV-1 could be the effect of the Vpu protein of HIV-1, which has previously been shown to cause such a modest reduction in cell surface MHCII levels in monocytic cells (29).…”

Section: Hiv-1 Nef Reduces Cell Surface Mhcii Levels In Myeloid Cellsmentioning

confidence: 97%

HIV-1 Nef Promotes Endocytosis of Cell Surface MHC Class II Molecules via a Constitutive Pathway

Chaudhry

Verghese²,

Das³

et al. 2009

The Journal of Immunology

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HIV-1 Nef has been reported to disrupt MHC class II (MHCII)-mediated Ag presentation by a dual strategy that comprises a reduction in cell surface levels of peptide-loaded mature MHCII molecules and a up-regulation of immature MHCII molecules. We show that Nef achieves relocation of MHCII away from the cell surface in monocytic cells by both delaying its transport to the cell surface and by accelerating endocytic removal of cell surface MHCII to a lysosomal compartment. Nef-induced MHCII endocytosis is cholesterol-sensitive but clathrin- and dynamin-independent. Internalized MHCII molecules traverse the early endosomal system and colocalize with pinocytic cargo before reaching lysosomes. Nef-triggered MHCII endocytosis requires Rab5 activity and lyst function, whereas lysosomal trafficking of internalized MHCII molecules requires Rab7 activity. We further show that a similar pathway can remove peptide-MHCII complexes from the surface of monocytic cells not expressing Nef. Our data suggest that Nef uses mechanisms involved in normal MHCII recycling and turnover to mediate the delivery of cell surface MHCII to a lysosomal destination. Thus, Nef-mediated endocytosis of MHCII provides a novel perspective on the regulation of normal MHCII trafficking.

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“…Among others, the EBV EBNA1 protein contains an element that interferes with its proteasomal proteolysis, and the HSV ICP47 protein inhibits the TAP complex (31,32). HIV is highly efficient at evading immune responses through mechanisms such as modulation of MHC class II presentation (33) and downregulation of MHC class I molecules (3,(33)(34)(35). Many other viral immune evasion strategies are also described (36)(37)(38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Human EBV- and CMV-Specific Cytolytic Effector Function Using Allogeneic HLA Molecules

D’Orsogna

Heuvel

Meer-Prins

et al. 2012

The Journal of Immunology

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Viral infection is a major cause of morbidity and mortality, and there are few therapeutic options available to augment a virus-specific T cell response. Although allo-HLA cross-reactivity from virus-specific memory T cells is common, it is unclear whether priming with specific allogeneic cells could conversely elicit a viral peptide/self-HLA restricted cytotoxic T cell response in humans. First, we used the previously described allo-HLA-B*44:02 cross-reactivity of EBV peptide/HLA-B8 restricted T cells, to determine whether allogeneic HLA stimulation can elicit a cytolytic immune response against EBV. HLA-B8+ HLA-B44− EBV-seropositive PBMCs were stimulated with either HLA-B*44:02+ or HLA-B*44:03+ mismatched irradiated PBMCs in a 7–10 d MLR. The allo-HLA stimulated responder cells were then evaluated for cytotoxicity using EBV peptide loaded autologous target cells and unloaded HLA-B8+ EBV LCL target cells. PBMCs from EBV-seropositive donors gained EBV-specific cytolytic effector function following specific allo-HLA stimulation. Finally, we also elicited cytolytic CMV-specific responses using specific allogeneic cell stimulation, to confirm that this technique can be used to elicit viral peptide/self-HLA restricted responses even from nonpublic TCR responses. Allogeneic cell stimulation used as a cell therapy may be a potential tool to augment an antiviral T cell response in patients with EBV or CMV infection.

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Human Immunodeficiency Virus Type 1 Vpu Protein Interacts with CD74 and Modulates Major Histocompatibility Complex Class II Presentation

Cited by 52 publications

References 55 publications

Robust NK Cell-Mediated Human Immunodeficiency Virus (HIV)-Specific Antibody-Dependent Responses in HIV-Infected Subjects

Robust NK Cell-Mediated Human Immunodeficiency Virus (HIV)-Specific Antibody-Dependent Responses in HIV-Infected Subjects

HIV-1 Nef Promotes Endocytosis of Cell Surface MHC Class II Molecules via a Constitutive Pathway

Stimulation of Human EBV- and CMV-Specific Cytolytic Effector Function Using Allogeneic HLA Molecules

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