期刊
JOURNAL OF INFECTIOUS DISEASES
卷 212, 期 5, 页码 803-807出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiv114
关键词
XLP disease; EBV; 2B4; CD8(+) T cells; HIS mice
资金
- Cancer Research Switzerland [KFS-3234-08-2013]
- Worldwide Cancer Research [14-1033]
- University of Zurich
- Baugarten Foundation
- Sobek Foundation
- Fondation Acteria
- Swiss Vaccine Research Institute
- Swiss National Science Foundation [310030_143979, CRSII3_136241]
- German Research Foundation
- Associazione Italiana Ricerca per la Ricerca sul Cancro [9962, 15704]
- Progetto di Ricerca Fondazione Carige
- Progetto di Ricerca di Ateneo
- Swiss National Science Foundation (SNF) [310030_143979] Funding Source: Swiss National Science Foundation (SNF)
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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