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*
Viral Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke,
Experimental Immunology Branch and
Viral Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
Human T lymphotropic virus type I (HTLV-I)-associated
myelopathy/tropical spastic paraparesis (HAM/TSP) is an inflammatory
neurologic disease caused by HTLV-I infection and has been associated
with elevated levels of several proinflammatory cytokines in both serum
and cerebrospinal fluid. It is unknown what kind of cells secrete these
cytokines and if HTLV-I Ags are associated with this phenomenon. Here,
we investigated the expression of cytokines in PBL from eight HAM/TSP
patients, nine HTLV-I-infected asymptomatic carriers, and seven healthy
controls by flow cytometry combined with intracellular cytokine
staining. PBL were cultured with brefeldin A without mitogen and IL-2
for 14 h. Under these conditions, CD8+ cells produced
proinflammatory cytokines including IFN-
, TNF-
, and IL-2, which
were significantly elevated in HAM/TSP patients. The proportion of
CD8+ cells producing IFN- in HAM/TSP patients,
asymptomatic carriers, and healthy controls were, on average, 4.9, 0.4,
and 0.3%, respectively. IFN- production by these CD8+
cells was suppressed by anti-HLA-class I Ab. Purified
CD8+ cells from an HLA-A2 HAM/TSP patient produced IFN-
by cocultivation with autologous CD4 cells, the main reservoir of
HTLV-I in vivo, or allogenic HLA-A2+ B cells pulsed with a
known immunodominant HTLV-I tax peptide. These data suggest that high
levels of circulating HTLV-I-specific CD8+ T lymphocytes
have the potential to produce proinflammatory cytokines and may promote
inflammatory responses to HTLV-I in HAM/TSP
patients.
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