Selected article for: "a59 infection and MHC class"

Title: Coronavirus induction of class I major histocompatibility complex expression in murine astrocytes is virus strain specific
  • Document date: 1994_9_1
  • ID: 4bf8eiix_4
    Snippet: Currently, there is very little known about the ability of MHV strains to influence specific activities of the host cells that they infect. Early reports indicate that A59 infection enhances the expression of MHC class I molecules in primary cultures of murine glial cells (33) and that the enhancement also occurs in the brain after i.c. infection in C57B1/6 mice (34). Since class I molecules play a key role in the interaction between infected tar.....
    Document: Currently, there is very little known about the ability of MHV strains to influence specific activities of the host cells that they infect. Early reports indicate that A59 infection enhances the expression of MHC class I molecules in primary cultures of murine glial cells (33) and that the enhancement also occurs in the brain after i.c. infection in C57B1/6 mice (34). Since class I molecules play a key role in the interaction between infected target cells and CD8 + cytotoxic T cells (CTL; 35, 36) , any change in their expression after virus infection has potential implications for the outcome of the infection. Cells in the CNS generally express little, if any, constitutive class I antigen in vivo, but astrocytes have been consistently reported to express both class I and class II antigens in vitro after the addition of IFN-3' and/or TNF-ot to the culture medium (37) (38) (39) (40) (41) (42) . Several reports indicate that astrocytes are capable of acting as antigen-presenting cells for in vitro antigen-or a11ospecific CD4 § and CD8 § T cell responses (43, 44) , which suggests that they also have potential to participate in immune responses occurring within the confines of the CNS. Since clearance of infectious JHMV from the CNS requires class I-restricted CD8 + T cells (11, (45) (46) (47) , it is of particular interest to characterize the effect of MHV infection on class I expression in one of its principal cellular targets.

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