Effect of Friend Leukemogenic Virus on Antibody-Forming Cells to a Bacterial Somatic Antigen

• Published in: JNCI : Journal of the National Cancer Institute 1969-12, Vol.43 (6), p.1337-1345
• Main Authors: Hirano, Shinji, Ceglowski, Walter S., Allen, Jerry L., Friedman, Herman
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Antibody Formation; Antibody-Producing Cells; Antigen-Antibody Reactions; Antigens; Bacteriolysis; Escherichia coli - immunology; Female; Friend murine leukemia virus; Hemolytic Plaque Technique; Immunity, Cellular; Immunization; Leukemia, Experimental - immunology; Leukemia, Experimental - microbiology; Lipopolysaccharides; Mice; Polysaccharides, Bacterial; Spleen - immunology; Splenomegaly - immunology; Splenomegaly - microbiology; Time Factors
• ISSN: 0027-8874; 1460-2105
• DOI: 10.1093/jnci/43.6.1337

Adult BALB/c mice were infected with Friend leukemogenic virus (FLV) and tested for their ability to produce specific antibody-secreting cells to Escherichia coli after challenge immunization. A direct bacteriolytic plaque assay with viable E. coli as the indicator was used for the assay. Normal noninfected animals had a vigorous immune response after immunization with the lipopolysaccharide antigen derived from the bacteria. Mice infected with virus also responded with plaque-forming cells (PFC) to E. coli, but the magnitude of the response was markedly depressed. The time of virus infection relative to the day of immunization was an important factor, since the greatest suppression occurred in animals infected 3, 7, or 14 days before immunization. There was no significant suppression, and occasionally an enhancement, when mice were infected with virus 1 or 2 days after immunization. In general, the greatest depression was apparent, regardless of the day of immunization or infection, when the number of PFC was calculated per million leukocytes rather than per whole spleen. Serum agglutinin titers to E. coli were also suppressed in animals infected with the leukemia virus before immunization. The degree of suppression of the antibody titer was much less than that occurring on the cellular level. The number of “background” antibody-forming cells to E. coli was unaffected by infection with the leukemogenic virus. The degree of splenomegaly seemed related to the marked immunosuppression of induced antibody-forming cells to E. coli late in the infection.