Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.
An IFN-gamma-dependent pathway plays a critical role in the pathogenesis of murine immunodeficiency syndrome induced by LP-BM5 murine leukemia virus.
Int Immunol. 1994 Dec;6(12):1937-47. Unique Identifier : AIDSLINE MED/95210211 Uehara S; Hitoshi Y; Numata F; Makino M; Howard M; Mizuochi T; Takatsu K; Department of Immunology, University of Tokyo, Japan.
Abstract:
The murine acquired immunodeficiency syndrome (MAIDS) caused by a defective murine leukemia virus produces severe immunodeficiency with abnormal lymphoproliferation and hypergammaglobulinemia. The presence of both CD4+ T cells and B cells is critical for the development of this disease. Remarkably elevated mRNA expression for IFN-gamma and IL-10 was observed in spleen cells of C57BL/6 mice starting from the early phase of viral infection. IFN-gamma production was induced by spleen cells from virus-infected mice upon stimulation with concanavalin A or lipopolysaccharide in both the early and late phases of MAIDS progression. When mice that had been passively administered anti-IFN-gamma mAb were infected with the virus, the development and progression of lymphadenopathy, immunodeficiency and elevated levels of serum IgG2a associated with MAIDS were delayed. Treatment with anti-IL-4 or anti-IL-10 mAb in place of anti-IFN-gamma mAb did not induce the delayed progression of MAIDS. These data support the concept that IFN-gamma-dependent pathway may be involved in the development of MAIDS.
Keywords: Animal Antibodies, Monoclonal/IMMUNOLOGY Base Sequence Cells, Cultured Enzyme-Linked Immunosorbent Assay Female Flow Cytometry Interferon Type II/*IMMUNOLOGY Interleukin-10/IMMUNOLOGY Interleukin-4/IMMUNOLOGY Interleukins/*IMMUNOLOGY Leukemia Viruses, Murine Mice Mice, Inbred C57BL Molecular Sequence Data Murine Acquired Immunodeficiency Syndrome/*IMMUNOLOGY/VIROLOGY Polymerase Chain Reaction Support, Non-U.S. Gov't Th1 Cells/IMMUNOLOGY JOURNAL ARTICLE 950730
M9570934
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