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Characterization of measles virus-induced cellular autoimmune reactions against myelin basic protein in Lewis rats
U G Liebert1, G A Hashim, V ter Meulen
1Institut für Virologie und Immunobiologie, Universität Würzburg, F.R.G.
Abstract:
Subacute encephalomyelitis (SAME) in Lewis rats following infection with a neurotropic measles virus (MV) is associated with a cell-mediated autoimmune response (CMAI) to myelin basic protein (MBP). MBP-selected CD4+ T cell lines both from measles-infected animals as well as from rats challenged with guinea pig MBP (Gp-MBP) had a similar pattern of response in the presence of synthetic peptides to Gp-MBP and specifically responded in vitro only to the encephalitogenic and not the non-encephalitogenic or other control peptides. In primary splenic lymphocyte cultures from SAME animals, however, a low but significant T-cell response was obtained against the non-encephalitogenic peptide S67 (residues 69-81) of the Gp-MBP. Moreover, immunization of MV-infected rats with this peptide induced clinical and histological experimental allergic encephalomyelitis (EAE) in 38% of the animals. The results of the study show that the non-encephalitogenic peptide S67 can be rendered encephalitogenic in rats when an additional stimulus is given in the form of MV infection. The data indicate further that MV infection of the central nervous system (CNS) enhances the susceptibility of the CNS to autoimmune T cell aggression.
Insights
Measles virus infection can make a non-encephalitogenic myelin basic protein peptide cause experimental allergic encephalomyelitis (EAE) in rats. This suggests viral infections enhance central nervous system susceptibility to autoimmune T cell attacks.
Area of Science:
- Neuroimmunology
- Virology
- Autoimmunity
Background:
- Subacute encephalomyelitis (SAME) in Lewis rats is linked to a cell-mediated autoimmune response against myelin basic protein (MBP).
- CD4+ T cell lines from infected rats recognize specific encephalitogenic peptides of guinea pig MBP (Gp-MBP).
Purpose of the Study:
- To investigate if a non-encephalitogenic Gp-MBP peptide (S67) can induce experimental allergic encephalomyelitis (EAE) in the context of measles virus (MV) infection.
- To explore the role of MV infection in enhancing central nervous system (CNS) susceptibility to autoimmune T cell-mediated damage.
Main Methods:
- Generating and characterizing MBP-specific CD4+ T cell lines from MV-infected rats.
- Assessing T cell responses in vitro to synthetic Gp-MBP peptides.
- Immunizing MV-infected rats with the non-encephalitogenic peptide S67 and evaluating for EAE induction.
Main Results:
- A low but significant T cell response was observed against the non-encephalitogenic peptide S67 in primary splenic lymphocyte cultures from SAME animals.
- Immunization with peptide S67 in MV-infected rats induced clinical and histological EAE in 38% of the animals.
- MV infection rendered a typically non-encephalitogenic peptide capable of inducing EAE.
Conclusions:
- Measles virus infection can render a non-encephalitogenic peptide encephalitogenic in rats, suggesting a role for viral triggers in autoimmunity.
- MV infection of the CNS appears to increase susceptibility to autoimmune T cell aggression, highlighting a mechanism for virus-induced neurological disease.