Role of antibody response helper factors in immunosuppressive effects of friend leukemia virus.
The primary antibody response of BALB/c splenocytes to sheep erythrocytes in vitro was suppressed by infection with Friend leukemia virus (FLV), with the response capacity decreasing with increasing duration of infection. The acquisition of normal antibody responses was amplified by macrophage-produced antibody response helper factor(s). FLV-infected mice were treated with bacterial lipopolysaccharide to induce the release of these helper factors into the serum. Similar to the loss of antibody response capacity by their splenocytes, the FLV-infected mice progressively lost the ability to produce helper factors in response to lipopolysaccharide. In vitro cultures of FLV-infected cells also showed a depressed ability to produce helper factor activity both spontaneously and in response to lipopolysaccharide stimulation. The reconstitution of normal levels of exogenous helper factors to FLV-infected splenocytes restored the antibody response to normal or even elevated levels. These studies indicate that the mechanism for suppression of antibody responses by FLV involves the depression of antibody response helper factor production.
D000818:Animals; D000917:Antibody Formation; D005622:Friend murine leukemia virus / Q000276:immunology*; D007108:Immune Tolerance; D007942:Leukemia, Experimental / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D006377:T-Lymphocytes, Helper-Inducer / Q000502:physiology*
D008070:Lipopolysaccharides