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- Scopus: eid_2-s2.0-0030876983
- PMID: 9251680
- WOS: WOS:A1997XN86100007
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Article: Interferon α/β mediates early virus-induced expression of H-2D and H-2K in the central nervous system
Title | Interferon α/β mediates early virus-induced expression of H-2D and H-2K in the central nervous system |
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Authors | |
Issue Date | 1997 |
Citation | Laboratory Investigation, 1997, v. 77, n. 1, p. 71-84 How to Cite? |
Abstract | Cells of the central nervous system (CNS) normally do not express detectable levels of major histocompatibility complex (MHC) Class I antigens. However, MHC Class I expression can be induced after virus infection. We tested the hypothesis that virus-induced Class I expression is mediated by lymphocytes or cytokines using lymphocyte- and cytokine-deficient mice. We used Theiler's murine encephalomyelitis virus (TMEV), which induces CNS demyelination that maps genetically to the D region of MHC Class I and is associated with high levels of Class I products. TMEV infection of severe combined immunodeficiency (SCID) and recombination activation gene-1- deficient mice, which lack B and T lymphocytes, resulted in equivalent H-2D and H-2K expression in brain and spinal cord, according to analysis of the area and intensity of immunoperoxidase staining. Class I antigens were demonstrated as early as 6 hours after infection, and they were more widely distributed than vital RNA, indicating that expression was induced indirectly via a soluble factor. To determine whether cytokines induced the expression, we infected mice lacking receptors for interferon-α/β (IFN-α/βR(-/-)), interferon-γ (IFN-γR(-/-)), and tumor necrosis factor-α (TNFRp55(-/-)). TMEV-infected IFN-γR(-/-) and TN-FRp55(-/-) mice expressed Class I antigens in the CNS, whereas IFN-α/βR(-/-) mice did not, establishing that IFN- α/β mediated the expression. In contrast to the equivalent expression in SCID mice, we observed greater area and higher intensity of H-2D versus H-2K antigens in infected SCID mice reconstituted with normal spleen cells. Collectively, the data indicate that after TMEV infection, early generalized MHC Class I expression is mediated by IFN-α/β independently of lymphocytes, but the differential regulation of H-2D over H-2K may be controlled by B and/or T lymphocytes. |
Persistent Identifier | http://hdl.handle.net/10722/291409 |
ISSN | 2023 Impact Factor: 5.1 2023 SCImago Journal Rankings: 1.243 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Njenga, M. Kariuki | - |
dc.contributor.author | Pease, Larry R. | - |
dc.contributor.author | Wettstein, Peter | - |
dc.contributor.author | Mak, Tak | - |
dc.contributor.author | Rodriguez, Moses | - |
dc.date.accessioned | 2020-11-17T14:54:18Z | - |
dc.date.available | 2020-11-17T14:54:18Z | - |
dc.date.issued | 1997 | - |
dc.identifier.citation | Laboratory Investigation, 1997, v. 77, n. 1, p. 71-84 | - |
dc.identifier.issn | 0023-6837 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291409 | - |
dc.description.abstract | Cells of the central nervous system (CNS) normally do not express detectable levels of major histocompatibility complex (MHC) Class I antigens. However, MHC Class I expression can be induced after virus infection. We tested the hypothesis that virus-induced Class I expression is mediated by lymphocytes or cytokines using lymphocyte- and cytokine-deficient mice. We used Theiler's murine encephalomyelitis virus (TMEV), which induces CNS demyelination that maps genetically to the D region of MHC Class I and is associated with high levels of Class I products. TMEV infection of severe combined immunodeficiency (SCID) and recombination activation gene-1- deficient mice, which lack B and T lymphocytes, resulted in equivalent H-2D and H-2K expression in brain and spinal cord, according to analysis of the area and intensity of immunoperoxidase staining. Class I antigens were demonstrated as early as 6 hours after infection, and they were more widely distributed than vital RNA, indicating that expression was induced indirectly via a soluble factor. To determine whether cytokines induced the expression, we infected mice lacking receptors for interferon-α/β (IFN-α/βR(-/-)), interferon-γ (IFN-γR(-/-)), and tumor necrosis factor-α (TNFRp55(-/-)). TMEV-infected IFN-γR(-/-) and TN-FRp55(-/-) mice expressed Class I antigens in the CNS, whereas IFN-α/βR(-/-) mice did not, establishing that IFN- α/β mediated the expression. In contrast to the equivalent expression in SCID mice, we observed greater area and higher intensity of H-2D versus H-2K antigens in infected SCID mice reconstituted with normal spleen cells. Collectively, the data indicate that after TMEV infection, early generalized MHC Class I expression is mediated by IFN-α/β independently of lymphocytes, but the differential regulation of H-2D over H-2K may be controlled by B and/or T lymphocytes. | - |
dc.language | eng | - |
dc.relation.ispartof | Laboratory Investigation | - |
dc.title | Interferon α/β mediates early virus-induced expression of H-2D and H-2K in the central nervous system | - |
dc.type | Article | - |
dc.identifier.pmid | 9251680 | - |
dc.identifier.scopus | eid_2-s2.0-0030876983 | - |
dc.identifier.volume | 77 | - |
dc.identifier.issue | 1 | - |
dc.identifier.spage | 71 | - |
dc.identifier.epage | 84 | - |
dc.identifier.isi | WOS:A1997XN86100007 | - |
dc.identifier.issnl | 0023-6837 | - |