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

Obinna Chijioke; Emanuela Marcenaro; Alessandro Moretta; Riccarda Capaul; Christian Münz

doi:10.1093/infdis/jiv114

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

Obinna Chijioke, Emanuela Marcenaro, Alessandro Moretta, Riccarda Capaul, Christian Münz

Research output: Contribution to journal › Article › peer-review

33 Scopus citations

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.

Original language	English
Pages (from-to)	803-807
Number of pages	5
Journal	Journal of Infectious Diseases
Volume	212
Issue number	5
DOIs	https://doi.org/10.1093/infdis/jiv114
State	Published - 1 Sep 2015
Externally published	Yes

Keywords

2B4
CD8 T cells
EBV
HIS mice
XLP disease

Access to Document

10.1093/infdis/jiv114

Cite this

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title = "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",

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.",

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T1 - 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

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AU - Marcenaro, Emanuela

AU - Moretta, Alessandro

AU - Capaul, Riccarda

AU - Münz, Christian

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AB - 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.

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