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Virus-specific and autoreactive T cell lines isolated from cerebrospinal fluid of a patient with chronic rubella panencephalitis()

Using a recently described technique for expanding of human T lymphocyte populations from cerebrospinal fluid (CSF), we investigated the local cellular immune response in a patient with chronic rubella panencephalitis. A total of 328 T cell lines (TCLs) was established by seeding CSF cells at limiti...

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Detalles Bibliográficos
Autores principales: Martin, Roland, Marquardt, Peter, O'Shea, Siobhan, Borkenstein, Martin, Kreth, Hans W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier B.V. 1989
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119901/
https://www.ncbi.nlm.nih.gov/pubmed/2470776
http://dx.doi.org/10.1016/0165-5728(89)90065-9
Descripción
Sumario:Using a recently described technique for expanding of human T lymphocyte populations from cerebrospinal fluid (CSF), we investigated the local cellular immune response in a patient with chronic rubella panencephalitis. A total of 328 T cell lines (TCLs) was established by seeding CSF cells at limitin dilution into histoplates in the presence of irradiated feeder cells and phytohemagglutinin (PHA)-containing conditioned medium. 80% of TCLs expressed the CD4(+) CD8(−), 5% the CD4(−) CD8(+) phenotype and 15% of TCLs contained different proportions of CD4(+) and CD8(+) cells. Of 191 TCLs analyzed, 85 were cytotoxic, as shown by their lectin-dependent cytotoxicity against allogeneic uninfected target cells. Eight of them demonstrated specificity for the autologous, rubella virus-infected target cells. When testes for antigen-specific proliferative activity, 26 TCLs responded to rubella antigen, 16 TCLs reacted to myelin basic protein (MBP), four TCLs to proteolipid protein (PLP), four to galactocerebrosides and two to actin. Fourteen out of 16 MBP-specific TCLs also responded, to a minor degree, to rubella antigen and/or actin. The results showed that the persisting rubella infection had given rise to autoreactive T cells. Virus-induced autoreactivity to brain antigens may be an important pathogenic mechanism in other chronic inflammatory disorders of the CNS.