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Blood, 15 May 2001, Vol. 97, No. 10, pp. 3177-3183
IMMUNOBIOLOGY
Impaired production of naive T lymphocytes in human T-cell
leukemia virus type I-infected individuals: its implications in the
immunodeficient state
Jun-ichirou Yasunaga,
Tatsunori Sakai,
Kisato Nosaka,
Ken-ichiro Etoh,
Sadahiro Tamiya,
Shin Koga,
Shuji Mita,
Makoto Uchino,
Hiroaki Mitsuya, and
Masao Matsuoka
Opportunistic infections frequently occur in patients with adult
T-cell leukemia (ATL) and human T-cell leukemia virus type I (HTLV-I)
carriers. However, the underlying mechanisms of such infections remain
unknown. To clarify the mechanism of immunodeficiency in those infected
with HTLV-I, this study analyzed the T-cell subsets in HTLV-I carriers
and patients with HTLV-I-associated myelopathy/tropical spastic
paraparesis and ATL using 3-color fluorescence with CD62L and CD45RA
coexpression either with CD4+ or CD8+ T cells.
The number of naive T lymphocytes was markedly suppressed in patients
with ATL, particularly in those with acute form, compared with
uninfected control individuals. The number of naive T cells was low in
HTLV-I-infected individuals under 50 years old compared with
uninfected individuals, whereas the number of memory T lymphocytes was
greater in HTLV-I-infected individuals. Although the increase of
memory T lymphocytes correlated with HTLV-I provirus loads, no
relationship was found between naive T-cell counts and provirus loads.
T-cell receptor rearrangement excision circles (TRECs), which are
generated by DNA recombination during early T lymphopoiesis, were
quantified to evaluate thymic function in HTLV-I-infected individuals.
TREC levels were lower in HTLV-I-infected individuals than in
uninfected individuals. In HTLV-I carriers less than 70 years old, an
increase of Epstein-Barr virus DNA in peripheral blood mononuclear
cells was observed in 6 of 16 (38%) examined, whereas it was
detectable in only 1 of 11 uninfected controls. These results suggested
that the low number of naive T lymphocytes was due to suppressed
production of T lymphocytes in the thymus, which might account for
immunodeficiency observed in HTLV-I-infected individuals.
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