Infection of human T-lymphotropic virus type I to astrocytes in vitro with induction of the class II major histocompatibility complex
M Hirayama, T Miyadai, T Yokochi, K Sato, T Kubota… - Neuroscience …, 1988 - Elsevier
M Hirayama, T Miyadai, T Yokochi, K Sato, T Kubota, M Iida, N Fujiki
Neuroscience letters, 1988•ElsevierTo clarify the pathogenesis of human T-lymphotropic virus type I (HTLV-I)-associated
myelopathy (HAM), we examined whether HTLV-I infects normal human glial cells in vitro
with induction of the major histocompatibility complex (HMC) class II antigen by
immunofluorescence method. It was found that about 10% of astrocytes were infected with
HTLV-I with induction of class II MHC antigen. Fluorescence-conjugated HTLV-I was
adsorbed to 10% of astrocytes. On the contrary, there was no class II MHC antigen …
myelopathy (HAM), we examined whether HTLV-I infects normal human glial cells in vitro
with induction of the major histocompatibility complex (HMC) class II antigen by
immunofluorescence method. It was found that about 10% of astrocytes were infected with
HTLV-I with induction of class II MHC antigen. Fluorescence-conjugated HTLV-I was
adsorbed to 10% of astrocytes. On the contrary, there was no class II MHC antigen …
Abstract
To clarify the pathogenesis of human T-lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM), we examined whether HTLV-I infects normal human glial cells in vitro with induction of the major histocompatibility complex (HMC) class II antigen by immunofluorescence method. It was found that about 10% of astrocytes were infected with HTLV-I with induction of class II MHC antigen. Fluorescence-conjugated HTLV-I was adsorbed to 10% of astrocytes. On the contrary, there was no class II MHC antigen expression and very few HTLV-I infection on oligodendrocytes. We speculated that in patients with HAM, HTLV-I-specific, MHC class II antigen restricted, activated CD4+ cells could damage the MHC class II antigen + HTLV-I-infected astrocytes, leading to the disturbance of blood-brain barrier and to the destructive lesion in the central nervous system.
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