Flavivirus infection up-regulates the expression of class I and class II major histocompatibility antigens on and enhances T cell recognition of astrocytes in vitro

Abstract

West Nile virus (WNV) infection of astrocytes can up-regulate their expression of both class I and class II major histocompatibility complex (MHC) antigens as determined by flow cytometry with monoclonal antibodies specific for class I and class II MHC antigens. The up-regulation of class I MHC antigen expression could be partly caused by interferon secreted after WNV infection because the synthetic interferon inducer polyinosinic-polycytidylic acid (poly I:C) has similar effects. In contrast the up-regulation of class II MHC antigen expression was not induced by poly I:C. The increased MHC antigen expression by WNV infection had significant effects on T cell recognition. Thus, WNV and influenza virus A/WSN double-infected astrocytes but not astrocytes infected by A/WSN alone were lysed by influenza virus-immune cytotoxic T cells. Similarly, WNV-infected astrocytes were better stimulators than normal astrocytes for a class II MHC-reactive T cell line, both in terms of T cell proliferation and interleukin release.

Protection of adult but not newborn mice against lethal intracerebral challenge with Japanese encephalitis virus by adoptively transferred virus-specific cytotoxic T lymphocytes: requirement for L3T4+ T cells

“…lethal challenge with JEV and that complete protection can be achieved only by simultaneous presence of both Lyt 2.2 + (CD8 +) and L3T4 ~ (CD4 +) virus-specific T cells. It has been reported that both NK and Lyt 2 + cells can be isolated from the brains of mice infected with West Nile virus (WNV) (Liu et al, 1989). However, we observed protection of adult mice from JEV-induced mortality only by transferring the effectors by i.c.…”

Augmentation of major histocompatibility complex class I and ICAM‐1 expression on glial cells following measles virus infection: Evidence for the role of type‐1 interferon

“…As demonstrated here and elsewhere for MHC molecules [10][11][12]14] and for the firsttime for ICAM-1 (Table 2), it is apparent that enhanced expression may result from the virus infection itself, rather than in response to inflammatory cytokines. It is apparent moreover, that this has a functional impact in as much as an increased susceptibility Eur.…”

“…Release of type-1 IFN by virus-infected ce11s does not readily explain the low Ievel induction of MHC dass Il on astrocytes observed in some of our experiments and in studies by others [11,12,14]. Neutralizing antiborlies have been used [11] to exclude the role of IFN-y in virusmediated induction of MHC dass II although, as with the present studies with anti-type-1 IFN antibodies, such an approach cannot entirely exclude autocrine effects.…”

“…A number of reports have already been made regarding the up-regulation of MHC dass I on a variety of infected cell types ( [9][10][11][12], reviewed in [13]) and also MHC class II induction on otherwise negative cells, including astrocytes [11,12,14]. The mechanisms underlying the alteration of MHC expression in virus-infected cells are unclear.…”

CD8+T Cells Mediate Recovery andImmunopathology in West Nile VirusEncephalitis

“…For two reasons, it also seems improbable that the lack of ligand for CD4 ϩ T cells (MHC class II) is responsible for this CD8 ϩ T-cell predominance, as has been proposed by Liu et al (34). First, flavivirus infection upregulates class I but also class II MHC (35,36) on cells of the CNS. Furthermore, predominant CD4 ϩ T-cell infiltrates rather than CD8 ϩ T-cell infiltrates are observed in other encephalitic etiologies, such as experimental allergic encephalomyelitis (1,27).…”