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Flavivirus infection modulates cell surface MHC antigen expression of astrocytes
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data indlcate that B-cell response in Lyme disease with neurological manlfestations is compartmentalized to CSF. No correlation was found between numbers of cells producing specific antlbodies and levels of corresponding free antibodies as determined by ELISA. It is concluded that documentation of speciflc antibody production on single cell level is a new and feasible tool for evaluatlon of B-cell response in inflammatory nervous system diseases. i. Henriksson A, Link H, Cruz M and Stiernstedt G. Immunoglobulin abnormalities in cerebrospinal fluid and blood over the course of menlngoradiculitis (Bannwarth's syndrome). Ann Neurol 20:337-345, 1986.
Flavivirus
Infection Modulates Cell Surface MHC AntiKen Expression of Astrocytes 11
Y. Liu, N. King, A. Kesson, R.V. Blanden, A. Mullbacher, Department of Microbiology, The John Curtin School of Medical Research, The Australian National University, G.P.O. Box 334, Canberra, ACT 2601, Australia To study the pathogenesis of flavivirus infection of the central nervous system, neural cell cultures of ~95~ astrocytes were prepared from one-day-old CBA/H (H-2 ~) mice. West Nile virus productively infected such cultures and concomitantly induced interferon (IFN). Viral titers reach plateau levels at 48 hr after infection. No loss of cell viability was observed over a 2-wk period. The expression of cell surface class I and class II MHC antigens was analysed with McAbs and FACS. A significant increase in class I MHC antigen of the whole cell population and an increase in class II in I0-20Z of the cells was observed. Poly I : C induced IFN production in astrocytes and caused an increase in class I but not class II MHC antigens. A temperature-sensitive mutant of Kunjin virus (ts3, RNAmutant), though unable to cause productive infection in the astrocyte cell culture, induced IFN production and a concomitant increase of class I MHC antigen expression. These data suggest that the up-regulation of class I MHC antigen by flavivirus infection is at least partly a result of the I ~ produced, while that of class II MHC antaigen is IFN independent. In addition to the serological data, flavivirus infected CBA/H ~strocytes were significantly better at stimulating an IK-specific alloreactive T cell line (BI0.T6R(DdlqKq) anti-B10.AQR (DdlkKq) as compared to uninfected astrocytes. The proliferation response as well as interleukin-2 (IL-2) release from this T cell line were significantly elevated. IL-2 release and proliferation of the T cell line were inhibited by Ik-specific monoclonal antibody. Thus the changes of MHC antigen expression of flavivirus-infected astrocytes may have profound implications in T cell-mediated immune responses.
data indlcate that B-cell response in Lyme disease with neurological manlfestations is compartmentalized to CSF. No correlation was found between numbers of cells producing specific antlbodies and levels of corresponding free antibodies as determined by ELISA. It is concluded that documentation of speciflc antibody production on single cell level is a new and feasible tool for evaluatlon of B-cell response in inflammatory nervous system diseases. i. Henriksson A, Link H, Cruz M and Stiernstedt G. Immunoglobulin abnormalities in cerebrospinal fluid and blood over the course of menlngoradiculitis (Bannwarth's syndrome). Ann Neurol 20:337-345, 1986.
Flavivirus
Infection Modulates Cell Surface MHC AntiKen Expression of Astrocytes 11
Y. Liu, N. King, A. Kesson, R.V. Blanden, A. Mullbacher, Department of Microbiology, The John Curtin School of Medical Research, The Australian National University, G.P.O. Box 334, Canberra, ACT 2601, Australia To study the pathogenesis of flavivirus infection of the central nervous system, neural cell cultures of ~95~ astrocytes were prepared from one-day-old CBA/H (H-2 ~) mice. West Nile virus productively infected such cultures and concomitantly induced interferon (IFN). Viral titers reach plateau levels at 48 hr after infection. No loss of cell viability was observed over a 2-wk period. The expression of cell surface class I and class II MHC antigens was analysed with McAbs and FACS. A significant increase in class I MHC antigen of the whole cell population and an increase in class II in I0-20Z of the cells was observed. Poly I : C induced IFN production in astrocytes and caused an increase in class I but not class II MHC antigens. A temperature-sensitive mutant of Kunjin virus (ts3, RNAmutant), though unable to cause productive infection in the astrocyte cell culture, induced IFN production and a concomitant increase of class I MHC antigen expression. These data suggest that the up-regulation of class I MHC antigen by flavivirus infection is at least partly a result of the I ~ produced, while that of class II MHC antaigen is IFN independent. In addition to the serological data, flavivirus infected CBA/H ~strocytes were significantly better at stimulating an IK-specific alloreactive T cell line (BI0.T6R(DdlqKq) anti-B10.AQR (DdlkKq) as compared to uninfected astrocytes. The proliferation response as well as interleukin-2 (IL-2) release from this T cell line were significantly elevated. IL-2 release and proliferation of the T cell line were inhibited by Ik-specific monoclonal antibody. Thus the changes of MHC antigen expression of flavivirus-infected astrocytes may have profound implications in T cell-mediated immune responses.