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*
Department of Oncology and Surgical Sciences, Interuniversity Center for Research on Cancer, and
Institute of Neurology, University of Padua, and
Istituto Scientifico Tumori Biotechnology Section, Padua; and
§
Laboratorio Farmaceutico Lofarma, Milan, Italy
Intraperitoneal transfer of PBMC from EBV+ donors
into SCID mice leads to high human Ig levels in mouse serum and B cell
lymphoproliferative disease. As these events depend on the activation
of coinjected human T cells, we addressed the behavior of the Th1 and
Th2 subsets in this model. Production of IFN-
, but not of Th2
cytokines such as IL-4, was detected in culture supernatants of PBMC
stimulated in vitro with mouse splenocytes. Moreover, anti-CD3
stimulation of the human cells recovered from mice brought about
IFN-, but not IL-4, synthesis; on the other hand, PCR and in situ
hybridization analysis of ex vivo-recovered cells disclosed the
presence of mRNA for both cytokines following in vitro restimulation,
thus suggesting post-transcriptional regulation of IL-4 gene
expression. When SCID mice were inoculated with PBMC from atopic
donors, whose Th1/Th2 profile displays an imbalance toward Th2 cells,
tumor development rates were lower, and tumor latency was higher,
compared with those in mice injected with PBMC from normal donors.
Isotypic analysis of human Ig in mouse serum showed the exclusive
presence of IFN--driven IgG subclasses; in addition, human IgE were
low or undetectable in most cases. These findings indicate that
following transfer into SCID mice, human Th1 lymphocytes undergo
preferential activation, whereas Th2 function is down-regulated. Th1
lymphocytes probably are a major component in promoting
EBV+ B cell expansion and tumor development; the individual
Th1/Th2 profile could in part account for the as yet unexplained donor
variability in tumor generation in this experimental model.
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