Abstract
Defects in immune surveillance mechanisms may allow increased replication of human T-lymphotropic virus type I (HTLV-I) in peripheral blood mononuclear cells in HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP). To explore this possibility, antibody-dependent cell-mediated cytotoxicity (ADCC) against HTLV-I infected cells in HAM/TSP and in asymptomatic HTLV-I-seropositive carriers (SPC), was studied. ADCC activity was significantly depressed in HAM/TSP compared to SPC subjects (p < 0.025) and was due to specific reduction in ADCC effector activity. On the other hand, there was no difference in antibody component of anti-HTLV-I ADCC (ADCC-Ab) activities between HAM/TSP and SPC, although patients with more severe forms of disease tended to have higher anti-HTLV-I ADCC-Ab activity. In HAM/TSP, depressed ADCC activity against HTLV-I due to reduced ADCC-effector activity may allow increased replication of HTLV-I which may implicate the development of inflammatory neuropathologic lesions of HAM/TSP.
Original language | English |
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Pages (from-to) | 65-69 |
Number of pages | 5 |
Journal | Journal of the neurological sciences |
Volume | 142 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 1996 Oct |
Externally published | Yes |
Keywords
- ADCC
- HAM
- HTLV-I
- TSP
- cytotoxicity
- host defense
- immune surveillance
- retrovirus
ASJC Scopus subject areas
- Neurology
- Clinical Neurology