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An IFN-γ-dependent pathway plays a critical role in the pathogenesis of murine immunodeficiency syndrome induced by LP-BM5 murine leukemia virus
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1994
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ImmunodeficienciesImmune RegulationImmunologyImmunodominanceIfn-γ-dependent PathwayImmune SystemImmunotherapyMurine Immunodeficiency SyndromeHuman RetrovirusCritical RolePrimary ImmunodeficiencyAllergyAutoimmune DiseaseSevere ImmunodeficiencyAutoimmunityImmunologic DiseaseChronic Viral InfectionHivCell BiologyImmune Cell DevelopmentAntiviral ResponseMaids ProgressionMedicineViral ImmunityImmunodeficiency Syndrome
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.