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
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
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