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Blood, 1 August 2001, Vol. 98, No. 3, pp. 721-726
IMMUNOBIOLOGY
High production of interferon  but not interleukin-2
by human T-lymphotropic virus type I-infected peripheral blood
mononuclear cells
Emmanuel Hanon,
Peter Goon,
Graham P. Taylor,
Hitoshi Hasegawa,
Yuetsu Tanaka,
Jonathan N. Weber, and
Charles R. M. Bangham
From the Departments of Immunology and Genito-Urinary
Medicine and Communicable Diseases, Imperial College School of
Medicine, St Mary's Campus, London, United Kingdom; the First
Department of Internal Medicine, Ehime University School of Medicine,
Shigenobu, Ehime, Japan; and the Department of Infectious Disease and
Immunology, Okinawa-Asia Research Center of Medical Science, Faculty of
Medicine, University of The Ryukyus, Nishihara, Okinawa, Japan.
The transactivator protein of human
T-lymphotropic virus I (HTLV-I), Tax, has been associated
with the up-regulation of several host cell genes, including
interleukin 2 (IL-2), the IL-2 receptor- (IL-2R) chain (CD25), interferon  (IFN-), and tumor necrosis factor (TNF). It
has been proposed that an IL-2/CD25 autocrine loop plays a part in
maintaining the very high proviral loads often found in HTLV-I
infection. Furthermore, abnormal production of inflammatory cytokines
might contribute to the pathogenesis of the inflammatory diseases
associated with HTLV-I infection. However, there has been no study of
the expression of these genes in freshly isolated peripheral blood
mononuclear cells (PBMCs) naturally infected with HTLV-I. In the
present study, flow cytometry was used to determine which cytokines are
produced by freshly isolated PBMCs that spontaneously express the
HTLV-I Tax protein. Surprisingly, the results show that intracellular
Tax expression is associated with rapid up-regulation of IFN- but
not TNF or IL-2. A proportion of HTLV-I-infected cells express both
IFN- and the surface markers of effector memory cells. Such cells
are capable of migration through peripheral tissues and could therefore contribute to the inflammation seen in diseases such as
HTLV-I-associated myelopathy/tropical spastic paraparesis.
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