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Blood, 1 January 2002, Vol. 99, No. 1, pp. 224-231
IMMUNOBIOLOGY
Human T-cell leukemia virus type 2 induces survival and
proliferation of CD34+ TF-1
cells through activation of STAT1 and
STAT5 by secretion of interferon- and granulocyte
macrophage-colony-stimulating factor
Chiara Bovolenta,
Elisabetta Pilotti,
Massimiliano Mauri,
Marco Turci,
Paolo Ciancianaini,
Paola Fisicaro,
Umberto Bertazzoni,
Guido Poli, and
Claudio Casoli
From the AIDS Immunopathogenesis Unit, San Raffaele
Scientific Institute, Milan, Italy; the Institute of Medical Pathology,
University of Parma, Italy; and the Department of Mother and Child,
Biology and Genetic Section, University of Verona, Italy.
Human T-cell leukemia-lymphoma virus (HTLV) type-2 can induce the
survival and proliferation of CD34+ TF-1 cells deprived of
interleukin (IL)-3. This effect did not require productive infection
and occurred when HTLV-2 was produced from T cells (CMo), but not from
B cells (BMo), unless the latter virus was complexed with anti-HLA-DR
monoclonal antibodies (mAbs). Cellular and molecular mechanisms
triggered by HTLV-2 interaction with TF-1 cells were here investigated.
Activation of signal transducer and activator of transcription (STAT) 5 protein occurred in TF-1 cells incubated either with IL-3 or with
HTLV-2/CMo; in addition the virus, but not IL-3, activated STAT1. The
effect of HTLV-2 required several hours, suggesting dependence on the
induction of cellular factors. By screening a panel of secreted
factors, granulocyte macrophage-colony-stimulating factor (GM-CSF),
interferon (IFN)- , and stem cell factor (SCF) were found induced by
HTLV-2 in TF-1 cells. Of note is the fact that these molecules induce a
variety of biologic effects through the activation of STAT proteins, including STAT1 and STAT5. Neutralization experiments indicated that
GM-CSF and IFN-, but not SCF, were responsible for HTLV-2-induced STAT activation, whereas anti-GM-CSF antibodies greatly inhibited TF-1
cell proliferation. Finally, incubation of BMo virus with anti-HLA-DR
mAb rescued TF-1 cell survival in the absence of IL-3. Thus, HTLV-2
interaction with CD34+ precursor cells may lead to the
expression of cytokines that, by inducing autocrine activation of
STATs, may influence the host's regenerative capacity and immune
response to HTLV-2 and to other infectious agents.
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