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)

Citation
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
Citations number
38
Categorie Soggetti
Immunology
Journal title
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
ISSN journal
00099104 → ACNP
Volume
120
Issue
2
Year of publication
2000
Pages
307 - 316
Database
ISI
SICI code
0009-9104(200005)120:2<307:FRMDIP>2.0.ZU;2-D
Abstract
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.