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

Abstract

An intracellular staining procedure for the cytoskeletal marker, glial fibrillary acidic protein of astrocytes, has been developed which allows flow cytometric phenotyping of astrocytes within complex mixttires of glial cells. Employing this technique, we show here that measles virus infection of rat mixed gl.ial cell cultures results in a rapid augmentation of major histocompatibility complex (MHC) dass I and ICAM-1 on the majority of astrocytes in culture. MHC class I Ievels are increased on macrophages/microglia but ICAM-1 expression is not normally affected on this cell type. Some MHC dass II induction is also observed after virus infection but only on astrocytes. A type-I interferon (IFN)-inducible protein, Mx, was identified in cultured glial cells after infection. Qualitatively comparable MHC dass I and ICAM-1 enhancement after addition of type-I IFN, supports the conclusion that this cytokine(s) releasedas a result ofvirus infection, is responsible for alterations in the expression of molecules on glial cells, that are involved in T cell recognition. Astrocytes after viral infection were more susceptible to alloantigen-specific cytotoxic T lymphocytes and cytotoxic T lymphocyte activity was substantially reduced in the presence of mAb specific for MHC class I, ICAM-1 and LFA-1 but not MHC dass II. The relevance of these findings toT cell recognition of virus-infected cells in the centrat nervaus system is discussed.

Measles virus hemagglutinin mediates monocyte aggregation and increased adherence to measles-infected endothelial cells

“…Values indicate % of cells in aggregates and α 5 β 1 integrins on lymphocytes [7]. MV infection has been shown to augment ICAM-1 expression on glial cells [17]. In a previous paper, infection of monocytes with the Edmonston strain of MV was shown to lead to increased expression of LFA-1, which was also shown to mediate homotypic aggregation in MV-infected monocyte cultures [2].…”

Induction of the Mx protein of rainbow trout Oncorhynchus mykiss in vitro and in vivo with poly I:C dsRNA and infectious hematopoietic necrosis virus

“…Immunoassays have been developed to detect human Mx in blood (Towbin et al 1992, Oh et al 1994, and Mx has been used as a marker for IFN therapy ). Because of these properties, mammalian Mx protein has been used in several studies as a marker for type I IFN (Kraus et al 1992, Yamada et al 1994, Abrams et al 1995. Roers et al (1994) used the presence of Mx, and therefore type I IFN, to assess vaccination efficacy of attenuated yellow fever virus in volunteers.…”

Distribution of ICAM-1 immunoreactivity during aging in the human orbitofrontal cortex

“…Furthermore, in human subjects, there seems to be an age-related increase in astrocytic GFAP immunoreactivity in the cerebral cortex (Miguel-Hidalgo et al, 2000;Nichols et al, 1993;Prolla and Mattson, 2001;Si et al, 2004;Sykova et al, 1998) that might be paralleled by changes in key inflammatory molecules, particularly ICAM-1. In fact, astrocytes express ICAM-1 immunoreactivity in vitro and in vivo following brain damage (Aloisi et al, 1992;Kim, 1996;Kraus et al, 1992;Lee and Benveniste, 1999;Nordal and Wong, 2004;Olschowka et al, 1997;Shrikant et al, 1995;Weber et al, 1994).…”