Frequent reversible membrane damage in peripheral blood B cells in human Tcell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP)
Y. Furukawa et al., Frequent reversible membrane damage in peripheral blood B cells in human Tcell lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP), CLIN EXP IM, 120(2), 2000, pp. 307-316
Apoptosis in peripheral blood lymphocyte populations in HTLV-I-infected peo
ple in vivo was examined, to study the lymphocyte dynamics in HTLV-I infect
ion. Freshly isolated lymphocytes from 10 non-infected healthy people, eigh
t asymptomatic HTLV-I carriers and 15 patients with HAM/TSP were stained wi
th FITC-labelled annexin V to detect phosphatidylserine (PS) residue exposu
re at the outer plasma membrane leaflet as an early marker of apoptosis. Th
ere was no significant difference in annexin V positivity in CD4(+) and CD8
(+) lymphocytes between non-infected subjects, asymptomatic carriers and HA
M/TSP patients, but there was a greatly increased exposure of PS on CD19(+)
lymphocytes (B cells) detected by FITC-annexin V in 12 out of 15 (80%) HAM
/TSP patients, while only two out of eight (25%) asymptomatic carriers and
none of the non-infected healthy people showed this aberrant PS exposure on
B cells. The intensity of annexin V staining of B cells in HAM/TSP was int
ermediate, as distinct from the high annexin V staining on advanced apoptot
ic cells. However, annexin V positivity was decreased when the cells were s
tained after 24 h of culture, suggesting that the intermediate PS exposure
on the B cell in HAM/TSP is not a consequence of an apoptotic process, but
rather reflects reversible membrane damage. B cells with PS exposure in viv
o might provide a site for coagulation and inflammation, and so contribute
to the pathogenesis of HAM/TSP and its complications.