4
Views
0
CrossRef citations to date
0
Altmetric
Research Article

Precursors of Borna Disease Virus-Specific T Cells in Secondary Lymphatic Tissue of Experimentally Infected Rats

, , &
Pages 325-335 | Published online: 10 Jul 2009

References

  • Bilzer T, Stitz L (1994). Immune-mediated brain atrophy: CD8+ T cells contribute to tissue destruction during Borna disease. J Immunol 153: 818–823.
  • Deschl U, Stitz L, Herzog S, Frese K, Rott R (1990). Determi-nation of immune cells and expression of major histo-compatibility complex class II antigen in encephalitic le-sions of experimental Boma disease. Acta Neuropathol (Berl) 81: 41–50.
  • Hausmann J, Hallensleben W, de la Torre JC, Pagenstecher A, Zimmermann C, Pircher H, Staeheli P (1999). T cell ignorance in mice to Borna disease virus can be over-come by peripheral expression of the viral nucleopro-tein. Proc Nati Acad Sci USA 96: 9769–9774.
  • Hickey WF, Hsu BL, Kimura H (1991). T-lymphocyte entry into the central nervous system. J Neurosci Res 28: 254–260.
  • Hirano N, Kao M, Ludwig H (1983). Persistent, tolerant or subacute infection in Borna disease virus-infected rats. J Gen Virol 64: 1521–1530.
  • Inaba K, Young JW, Steinman RM (1987). Direct activa-tion of CD8+ cytotoxic T lymphocytes by dendritic cells. J Exp Med 166: 182–194.
  • Irani DN, Griffin DE (1991). Isolation of brain parenchymal lymphocytes for flow cytometric analysis. J Immunol Methods 139: 223–231.
  • Lewis AJ, Whitton JL, Hatalski CG, Weissenbock H, Lipkin WI (1999). Effect of immune priming on Borna disease. J Virol 73: 2541–2546.
  • Matsumoto Y, Ohmori K, Fujiwara M (1992). Immune reg-ulation by brain cells in the central nervous system: mi-croglia but not astrocytes present myelin basic protein to encephalitogenic T cell under in vivo-mimicking con-ditions. Immunology 76: 209–216.
  • Mims CA (1960). Intracerebral injections and the growth of viruses in the mouse brain. Br J Exp Pathol 41: 52–59.
  • Narayan O, Herzog S, Frese K, Scheefers K, Rott R (1983a). Pathogenesis of Boma disease in rats: immune-mediated viral ophthalmoencephalopathy causing blindness and behavioral abnormalities. J Infect Dis 148: 305–315.
  • Narayan O, Herzog S, Frese K, Scheefers H, Rott R (1983b). Behavioral disease in rats caused by immunopatholog-ical responses to persistent boma virus in the brain. Science 220: 1401–1403.
  • Noske K, Bilzer T, Planz O, Stitz L (1998). Virus-specific CD4+ T cells eliminate Borna disease virus from the brain via induction of cytotoxic CD8+ T cells. J Virol 72: 4387–4395.
  • Oehen S, Brduscha-Riem K, Oxenius A, Odermatt B (1997). A simple method for evaluating the rejection of grafted spleen cells by flow cytometry and tracing adoptively transferred cells by light microscopy. J Immunol Meth-ods 207: 33–42.
  • Planz O, Bilzer T, Sobbe M, Stitz L (1993). Lysis of MHC class I-bearing cells in Boma disease virus-induced degenerative encephalopathy. J Exp Med 178: 163–174.
  • Planz O, Bilzer T, Stitz L (1995). I=unopathogenic role of T-cell subsets in Boma disease virus-induced progres-sive encephalitis. J Virol 69: 896–903.
  • Planz O, Dumrese T, Hulpiisch S, Schirle M, Stevanovic S, Stitz L (2001). A naturally processed rat major his-tocompatibility complex class I-associated viral peptide as target structure of boma disease virus-specific CD8+ T cells. J Biol Chem 276: 13689–13694.
  • Planz O, Stitz L (1999). Borna disease virus nucleoprotein (p40) is a major target for CD8(±)-T-cell-mediated im-mune response. J Virol 73: 1715–1718.
  • Richt JA, Schmeel A, Frese K, Carbone KM, Narayan O, Rott R (1994). Borna disease virus-specific T cells pro-tect against or cause i=unopathological Boma disease. J Exp Med 179: 1467–1473.
  • Richt JA, Stitz L, Deschl U, Frese K, Rott R (1990). Borna dis-ease virus-induced meningoencephalomyelitis caused by a virus-specific CD4+ T-cell mediated immune re-action. J Gen Virol 71: 2565–2573.
  • Richt JA, Stitz L, Wekerle H, Rott R (1989). Borna disease, a progressive meningoencephalomyelitis as a model for CD4+ T cell-mediated i=unopathology in the brain. J Exp Med 170: 1045–1050.
  • Rubin SA, Yednock TA, Carbone KM (1998). In vivo treat-ment with anti-alpha4 integrin suppresses clinical and pathological evidence of Borna disease virus infection. J Neuroimmunol 84: 158–163.
  • Sedgwick JD, Mössner R, Schwender S, Ter Meulen V, Mossner R (1991). Major histocompatibility complex-expressing nonhematopoietic astroglia cells prime only CD8+ T lymphocytes: astroglial cells as perpetuators but not initiators of CD4+ T cell responses in the central ner-vous system. J Exp Med 173: 1235-1246.
  • Sobbe M, Bilzer T, Go=e1 S, Noske K, Planz O, Stitz L (1997). Induction of degenerative brain lesions af-ter adoptive transfer of brain lymphocytes from Boma disease virus-infected rats: presence of CD8+ T cells and perforin mRNA. J Virol 71: 2400–2407.
  • Stitz L, Planz O, Bilzer T, Frei K, Fontana A (1991). Trans-forming growth factor-/3 modulates T cell-mediated encephalitis caused by Borna disease virus. Pathogenic importance of CD8+ cells and suppression of antibody formation. J Immunol 147: 3581-3586.
  • Stitz L, Sobbe M, Bilzer T (1992). Preventive effects of early anti-CD4 or anti-CD8 treatment on Boma disease in rats. J Virol 66: 3316–3323.
  • Stitz L, Soeder D, Deschl U, Frese K, Rott R (1989). In-hibition of immune-mediated meningoencephalitis in persistently Borna disease virus infected rats by cy-closporine A. J Immunol 143: 4250–4256.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.