Send to

Choose Destination
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

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


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.


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

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Silverchair Information Systems Icon for Zurich Open Access Repository and Archive
Loading ...
Support Center