APOPTOSIS OF T-LYMPHOCYTES IN THE SPINAL-CORD LESIONS IN HTLV-I-ASSOCIATED MYELOPATHY - A POSSIBLE MECHANISM TO CONTROL VIRAL-INFECTION IN THE CENTRAL-NERVOUS-SYSTEM

Citation
F. Umehara et al., APOPTOSIS OF T-LYMPHOCYTES IN THE SPINAL-CORD LESIONS IN HTLV-I-ASSOCIATED MYELOPATHY - A POSSIBLE MECHANISM TO CONTROL VIRAL-INFECTION IN THE CENTRAL-NERVOUS-SYSTEM, Journal of neuropathology and experimental neurology, 53(6), 1994, pp. 617-624
Citations number
43
Categorie Soggetti
Pathology,Neurosciences,"Clinical Neurology
ISSN journal
00223069
Volume
53
Issue
6
Year of publication
1994
Pages
617 - 624
Database
ISI
SICI code
0022-3069(1994)53:6<617:AOTITS>2.0.ZU;2-O
Abstract
Immunocytochemical staining of spinal cords from five autopsied patien ts with HAM/TSP was performed using the monoclonal antibody TIA-1, a m arker of cytotoxic T lymphocytes (CTL). Many TIA-1+, CD8+ cells are di stributed in active inflammatory lesions. The number of TIA-1+ cells i s related to the amount of HTLV-I proviral DNA in situ. The protein TI A-1 has been associated with the induction of apoptosis in target cell s. In active inflammatory lesions, we found cells undergoing apoptosis , most of them identified as helper-inducer CD45RO T lymphocytes, whic h were consistent with in vivo cellular tropism of HTLV-I in patients with HAM/TSP. These findings suggest that CTL-induced apoptosis of T l ymphocytes may be one of the possible mechanisms which eliminate HTLV- I-infected cells from the central nervous system. In addition, many T lymphocytes in the inflammatory lesions expressed bcl-2 oncoprotein, s uggesting that infiltrated T lymphocytes may be resistant to apoptosis . Expression of bcl-2 oncoprotein may explain the longstanding inflamm atory process in the central nervous system of HAM/TSP