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• W2018909554 abstract "Epstein–Barr virus (EBV)-positive B-cell lymphoproliferative disease (BLPD)-like lesions develop in severe combined immunodeficient (SCID) mice inoculated with peripheral blood mononuclear cells (PBMCs) from EBV-seropositive donors. We used this model to investigate the pathogenesis of EBV-associated BLPD. Tumour incidence fell from 81% to 11% when only B cells were inoculated, suggesting a key role for T cells in tumour formation. This was further underlined by the reduction in tumour incidence from 76% to 7% when PBMCs were depleted of CD4 positive (+ve) helper T cells. Tumour outgrowth was also reduced when PBMC were depleted of CD8 +ve, CD45RA +ve or CD45RO +ve T cells. The majority of PBMC-derived tumours analysed by reverse transcriptase–polymerase chain reaction (RT–PCR) expressed mRNA for interleukin (IL) 2, 4, 6, 10 and interferon (IFN) γ. This is the cytokine pattern seen in activated T cells and includes B-cell growth factors. In situ hybridization studies confirmed that the tumour cells themselves express the growth factors, which is consistent with autocrine-stimulated tumour growth. Our results suggest the following sequence of events: (1) T cells are essential for the initial outgrowth of tumorigenic EBV +ve B cells in vivo; (2) the neoplasm sustains its growth in an autocrine, cytokine-stimulated manner; and (3) established tumours become independent of T-cell help." @default.
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• W2018909554 date "2000-06-01" @default.
• W2018909554 modified "2023-10-14" @default.
• W2018909554 title "Essential role for T cells in human B-cell lymphoproliferative disease development in severe combined immunodeficient mice" @default.
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• W2018909554 doi "https://doi.org/10.1046/j.1365-2141.2000.02066.x" @default.
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