PDF《Antigen》

of August 22, 2018.

This information is current as Antigen Infected B Cells following Capture of BHRF1 EBV Lytic Protein BHRF1 by EBV Latently Long-Term MHC Class II Presentation of the Elisabeth Houssaint Elise Landais, Xavier Saulquin, Marc Bonneville and http://www.jimmunol.org/content/175/12/7939 doi: 10.4049/jimmunol.175.12.7939 2005;

175:7939-7946;

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2018 http://www.jimmunol.org/ Downloaded from Long-Term MHC Class II Presentation of the EBV Lytic Protein BHRF1 by EBV Latently Infected B Cells following Capture of BHRF1 Antigen1 Elise Landais, Xavier Saulquin, Marc Bonneville, and Elisabeth Houssaint2 Although T lymphocytes are considered essential for the control of EBV infection, it remains uncertain how this control occurs. We previously reported unexpected killing of EBV-transformed B-lymphoblastoid cells (LCLs) that did not express BHRF1 by CD4? T cells speci?c for BHRF1, an EBV lytic cycle protein. Using LCLs transformed with an EBV mutant, in which the BHRF1 gene was deleted, we showed that killing of latently infected cells through the recognition of a protein produced during the lytic cycle is due to transfer of BHRF1 from lytically infected to latently infected cells, which occurs in culture. Accordingly, LCLs ef?ciently presented exogenous BHRF1 protein. Furthermore, we present evidence for persistence of captured BHRF1 Ag for several days. Due to this long-term persistence, repeated loading of suboptimal amounts of BHRF1 led to accumulation of BHRF1 Ags in LCLs and, ultimately, to their optimal recognition by BHRF1-speci?c CD4? T cells. These results unveil an MHC class II-dependent pathway that could be important for the control of EBV latent infection through recognition of lytic cycle Ags. The Journal of Immunology, 2005, 175: 7939C7946. E pstein-Barr virus is a human ?-herpesvirus that latently infects ?95% of the population (1). The virus infects its host asymptomatically at a very young age and thereafter resides in the B cell population in a latent form (2). Although chronic EBV infection is free of complications in most individuals, EBV is, however, associated with lymphoid and epithelial cell tu- mors due to its cell transformation capacity (3). EBV is also an opportunistic agent often associated with malignancies occurring in immunosuppressed patients. This is the case for about half of B cell lymphomas developing in HIV-infected patients with a de- pleted CD4? T cell pool (4). Besides, post-transplant lymphopro- liferative diseases that occur sometimes upon immunosuppression are nearly always EBV associated (3). After primary infection, EBV is carried for life as a latent in- fection of the circulating memory B cell pool, with low level re- activation from latency into virus productive (lytic) infection at oropharyngeal sites. This virus encodes eight latent cycle proteins, the nuclear Ags EBV-encoded nuclear Ag