Walter S. Ceglowski

Suppression of the primary antibody plaque response of mice following infection with friend disease virus.

Summary Infection of mice with Friend Disease Virus prior to or simultaneous with immunization with sheep red blood cells resulted in a marked suppression of appearance of antibody forming cells, as determined by a localized hemolytic plaque technique in agar gel. Infection with virus had a marked suppressive effect on the number of 19S hemolysin forming cells in mouse spleen tissue at the peak of the expected immune response and during a period of two weeks or longer thereafter. Appearance of low efficiency 7S hemolysin forming cells late in the immune response, following a single injection of sheep red cells. Was also depressed in infected mice. Animals infected 3 days to a week or longer prior to immunization had the lowest number of detectable 19S or 7S antibody-forming cells. The number of plaque forming cells per million leukocytes tested was most suppressed in those mice which had obvious splenomegaly due to virus infection.

Leukemia Virus Suppression of Antibody-Forming Cells: Ultrastructure of Infected Spleens

Infection of adult BALB/c mice with Friend disease virus results in a leukemia-like disease characterized by erythropoietic changes and splenomegaly. A marked depression of formation of cellular and serum antibody occurs in infected animals. Electron-microscopic examination of the ultrastructure of spleen sections from infected mice with depressed immunity revealed that virus particles can be detected only in immature blastlike lymphoid cells and not in plasmocytes characteristic of the immune response in spleens of noninfected mice immunized with sheep erythrocytes.

Defect in Cellular Immunity of Leukemia Virus-Infected Mice Assessed by a Macrophage Migration-Inhibition Assay

Summary Cellular immunity in leukemic mice was studied using Friend leukemia virus and susceptible BALB/c mice. Injection of this virus into the test mice resulted in rapid development of splenomegaly and other symptoms of leukemia. There was a concomitant decrease in the ability of peritoneal cells from these animals to respond to PPD in vitro, as assessed by the macrophage migration-inhibition procedure. Sensitization of normal mice with mycobacteria in Freunds complete adjuvant resulted in rapid development of cellular immunity as assessed by the migration-inhibition assay. Failure to detect cellular immunity by this assay with peritoneal cells from leukemia virus-infected mice correlates with the marked decrease in humoral immunity, as well as cellular immunity previously assessed by skin graft rejection assays.

Calf thymus fractions: Enhancement and suppression of immunocompetent cells in neonatal mice

Nachweis, dass eine aus Kälber-Thymus isolierte Fraktion auf die Ausbildung von Hämolysin produzierenden Zellen in neugeborenen Mäusen einen stimulierenden Einfluss haben kann.

The Ultrastructure of Antibody-Forming Spleen Cells in Immunologically Suppressed Leukemic Mice

Previous studies in our laboratory and studies by others have demonstrated that infection with the murine leukemia viruses results in a significant depression in immunologic responsiveness (1,2). The extent of this suppression is dependent upon the dose of virus administered and the time interval between infection and immunization. These and other observations have been used to support the concept that there may be a competition between the leukemia virus and antigen for a limited number of precursor cells.

Immunosuppression by Tumor Viruses: Effects of Leukemia Virus Infection on the Immune Response**Some of the studies described here were supported by research grants from the U. S. National Science Foundation, the American Cancer Society, and the Damon Runyon Cancer Fund.

Publisher Summary This chapter discusses studies analyzing immunosuppression by tumor viruses, and the effects of leukemia virus infection on the immune response. In one study, mice infected with friend virus (FV) at different times, either prior to, simultaneously with, or after challenge immunization with sheep erythrocytes, showed varying levels of immunologic responsiveness. The fewest antibody plaque-forming cells (PFC) to the erythrocytes occurred in mice infected with virus prior to immunization. Maximum suppression occurred when the interval between infection and immunity was the longest. Both the primary and secondary responses were depressed when mice were infected with virus 3–8 days or longer before challenge immunization. Although both 7S (IgG) and 19S (IgM) PFCs were affected during the secondary response, the greatest depression occurred in the number of low-efficiency 7S PFCs. The degree of suppression was also directly related to the dose of virus administered. A greater level of immunosuppression occurred with the most concentrated dose of virus. Splenomegaly of infected animals appeared to be related to the level of immunosuppression.