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J Infect Dis. 2015 Sep 1;212(5):803-7. doi: 10.1093/infdis/jiv114. Epub 2015 Feb 26.

Role of the 2B4 Receptor in CD8+ T-Cell-Dependent Immune Control of Epstein-Barr Virus Infection in Mice With Reconstituted Human Immune System Components.

Author information

1
Viral Immunobiology, Institute of Experimental Immunology Institute of Surgical Pathology, University Hospital Zurich.
2
Deparment of Experimental Medicine Center of Excellence for Biomedical Research, University of Genoa, Italy.
3
Institute of Medical Virology, University of Zurich, Switzerland.
4
Viral Immunobiology, Institute of Experimental Immunology.

Abstract

Patients with X-linked lymphoproliferative (XLP) disease due to deficiency in the adaptor molecule signaling lymphocytic activation molecule-associated protein (SAP) are highly susceptible to one specific viral pathogen, the Epstein-Barr virus (EBV). This susceptibility might result from impaired CD8(+) T-cell and natural killer cell responses to EBV infection in these patients. We demonstrate that antibody blocking of the SAP-dependent 2B4 receptor is sufficient to induce XLP-like aggravation of EBV disease in mice with reconstituted human immune system components. CD8(+) T cells require 2B4 for EBV-specific immune control, because 2B4 blockade after CD8(+) T-cell depletion did not further aggravate symptoms of EBV infection.

KEYWORDS:

2B4; CD8+ T cells; EBV; HIS mice; XLP disease

PMID:
25722295
DOI:
10.1093/infdis/jiv114
[Indexed for MEDLINE]
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