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| 3. |
- Frisan, T, et al.
(författare)
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Generation of lymphoblastoid cell lines (LCLs)
- 2001
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Ingår i: Methods in molecular biology (Clifton, N.J.). - New Jersey : Humana Press. - 1064-3745. ; 174, s. 125-7
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Tidskriftsartikel (refereegranskat)
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| 4. |
- Frisan, T, et al.
(författare)
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Limiting dilution assay
- 2001
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Ingår i: Methods in molecular biology (Clifton, N.J.). - New Jersey : Humana Press. - 1064-3745. ; 174, s. 213-6
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Tidskriftsartikel (refereegranskat)
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| 5. |
- Frisan, T, et al.
(författare)
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Regression assay
- 2001
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Ingår i: Methods in molecular biology (Clifton, N.J.). - New Jersey : Humana Press. - 1064-3745. ; 174, s. 199-201
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Tidskriftsartikel (refereegranskat)
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| 6. |
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| 7. |
- Guerreiro-Cacais, AO, et al.
(författare)
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Capacity of Epstein-Barr virus to infect monocytes and inhibit their development into dendritic cells is affected by the cell type supporting virus replication
- 2004
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Ingår i: The Journal of general virology. - : Microbiology Society. - 0022-1317 .- 1465-2099. ; 85:Pt 10, s. 2767-2778
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Tidskriftsartikel (refereegranskat)abstract
- Epstein–Barr virus (EBV) is a ubiquitous human herpesvirus that is involved in the pathogenesis of a wide spectrum of malignant and non-malignant diseases. Strong evidence implicates T lymphocytes in the control of EBV replication and tumorigenesis, but cellular components of the innate immune system are poorly characterized in terms of their function in the development of EBV-specific immunity or interaction with the virus. This study demonstrates that EBV virions produced in epithelial cells surpass their B cell-derived counterparts in the capacity to enter monocytes and inhibit their development into dendritic cells (DCs). Different ratios of the gp42 and gH glycoproteins in the envelope of virions that were derived from major histocompatibility complex class II-positive or -negative cells accounted primarily for the differences in EBV tropism. EBV is shown to enter both monocytes and DCs, although the cells are susceptible to virus-induced apoptosis only if infected at early stages of DC differentiation. The purified gH/gL heterodimer binds efficiently to monocytes and DCs, but not to B cells, suggesting that high expression levels of a putative binding partner for gH contribute to virus entry. This entry takes place despite very low or undetectable expression of CD21, the canonical EBV receptor. These results indicate that the site of virus replication, either in B cells or epithelial cells, alters EBV tropism for monocytes and DCs. This results in a change in the virus's immunomodulating capacity and may have important implications for the regulation of virus–host interactions during primary and chronic EBV infection.
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| 16. |
- Li, LQ, et al.
(författare)
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Epstein-Barr virus inhibits the development of dendritic cells by promoting apoptosis of their monocyte precursors in the presence of granulocyte macrophage-colony-stimulating factor and interleukin-4
- 2002
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Ingår i: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 99:10, s. 3725-3734
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Tidskriftsartikel (refereegranskat)abstract
- Epstein-Barr virus (EBV) is a tumorigenic human herpesvirus that persists for life in healthy immunocompetent carriers. The viral strategies that prevent its clearance and allow reactivation in the face of persistent immunity are not well understood. Here we demonstrate that EBV infection of monocytes inhibits their development into dendritic cells (DCs), leading to an abnormal cellular response to granulocyte macrophage–colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4) and to apoptotic death. This proapoptotic activity was not affected by UV inactivation and was neutralized by EBV antibody-positive human sera, indicating that binding of the virus to monocytes is sufficient to alter their response to the cytokines. Experiments with the relevant blocking antibodies or with mutated EBV strains lacking either the EBV envelope glycoprotein gp42 or gp85 demonstrated that interaction of the trimolecular gp25–gp42–gp85 complex with the monocyte membrane is required for the effect. Our data provide the first evidence that EBV can prevent the development of DCs through a mechanism that appears to bypass the requirement for viral gene expression, and they suggest a new strategy for interference with the function of DCs during the initiation and maintenance of virus-specific immune responses.
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