Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Epstein-Barr Virus Evades CD4+ T Cell Responses in Lytic Cycle through BZLF1-mediated Downregulation of CD74 and the Cooperation of vBcl-2

22 Dec 2011

Abstract excerpt

Evasion of immune T cell responses is crucial for viruses to establish persistence in the infected host. Immune evasion mechanisms of Epstein-Barr virus (EBV) in the context of MHC-I antigen presentation have been well studied. In contrast, viral interference with MHC-II antigen presentation is less well understood, not only for EBV but also for other persistent viruses. Here we show that the EBV encoded BZLF1...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Eosinophilic Disorders and Syndromes
Share to Galectins and Cancer Biology
Share to Macrophage Migration Inhibitory Factor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 22216005
DOI: 10.1371/journal.ppat.1002455

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Epstein-Barr Virus Evades CD4+ T Cell Responses in Lytic Cycle through BZLF1-mediated Downregulation of CD74 and the Cooperation of vBcl-2PMID 22216005Read ↗

The Missing Link in Epstein-Barr Virus Immune Evasion: the BDLF3 Gene Induces Ubiquitination and Downregulation of Major Histocompatibility Complex Class I (MHC-I) and MHC-IISemantic proximity Read ↗

The Epstein-Barr Virus G-Protein-Coupled Receptor Contributes to Immune Evasion by Targeting MHC Class I Molecules for DegradationSemantic proximity Read ↗

The Lytic Cycle of Epstein-Barr Virus Is Associated with Decreased Expression of Cell Surface Major Histocompatibility Complex Class I and Class II MoleculesSemantic proximity Read ↗

The Immunomodulatory Capacity of an Epstein-Barr Virus Abortive Lytic Cycle: Potential Contribution to Viral TumorigenesisSemantic proximity Read ↗

EBV BILF1 evolved to downregulate cell surface display of a wide range of HLA class I molecules through their cytoplasmic tail.Semantic proximity Read ↗

Stage-specific inhibition of MHC class I presentation by the Epstein-Barr virus BNLF2a protein during virus lytic cycle.Semantic proximity Read ↗

Epstein-Barr viral miRNAs inhibit antiviral CD4+ T cell responses targeting IL-12 and peptide processingSemantic proximity Read ↗

Entry into the lytic cycle exposes EBV-infected cells to NK cell killing via upregulation of the MICB ligand for NKG2D and activation of the CD56bright and NKG2A+KIR+CD56dim subsetsSemantic proximity Read ↗

Epstein-Barr virus LMP2A suppresses MHC class II expression by regulating the B-cell transcription factors E47 and PU.1Semantic proximity Read ↗

Epstein–Barr virus‐encoded EBNA1 and ZEBRA : targets for therapeutic strategies against EBV ‐carrying cancersSemantic proximity Read ↗

The Epstein-Barr Virus-Encoded BILF1 Protein Modulates Immune Recognition of Endogenously Processed Antigen by Targeting Major Histocompatibility Complex Class I Molecules Trafficking on both the Exocytic and Endocytic PathwaysSemantic proximity Read ↗

Immune regulation in Epstein-Barr virus-associated diseasesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.