IgG Plaque-forming Cell Responses Research Articles

Chronic malarial infection in Balb/c mice. Effect on the immune response to sheep erythrocytes and histological changes in the liver and spleen

Chronic malarial infection was established in Balb/c mice by following Plasmodium berghei yoelii with P. b. berghei infection. It was found that the IgG plaque-forming cell response to sheep erythrocytes was depressed for at least six months. A preliminary investigation of the histological changes in the spleen and liver is described. The possibility that chronically infected mice could serve as a model for the tropical splenomegaly syndrome is discussed.

Immune responses in vitro. XI. Suppression of primary IgM and IgG plaque-forming cell responses in vitro by alloantisera against leukocyte alloantigens.

The effects of alloantisera against leukocyte alloantigens on plaque-forming cell (PFC) responses to sheep erythrocytes and the terpolymer of L-glutamic acid(60)-L-alanine(30)-L-tyrosine(10) (GAT) by mouse spleen cells in vitro have been investigated. Polyspecific antibodies against both H-2 and non-H-2 alloantigens on responding spleen cells suppressed both IgM and IgG PFC responses; antisera against alloantigens coded for by the K and I regions, but not the D region, of the H-2 complex also effectively suppressed PFC responses. The suppression was not due to cytotoxicity to the spleen cells or anti-immunoglobulin activity in the sera and was directly related to the amount of antiserum added to the cultures. The suppression was specific for spleen cells against which the alloantiserum was directed. The alloantisera suppressed responses most effectively when present during the first 24 h of incubation, and although not rendering lymphoid cells incapable of developing PFC responses after removal of noncell-bound antibody, did act by interfering with successful initiation of the PFC response. The alloantisera suppressed both IgM and IgG PFC responses when directed against alloantigens only on macrophages, but selectively suppressed IgG responses when directed against alloantigens only on lymphoid cells. The alloantisera did not interfere with the ability of macrophages to bind GAT or to support the viability of the lymphoid cells, but did interfere with the ability of macrophage-associated antigen to effectively stimulate antibody responses by the lymphoid cells. Possible mechanisms for the effects of alloantisera on macrophages and the selective suppression of IgG responses when the antisera are directed against alloantigens on lymphoid cells are discussed with reference to our current understanding of genetic restrictions governing cell interactions in the development of antibody responses in mice.

Immunocyte Response to a Purified Bacterial Toxin (Choleragen) and Toxoid: Cytokinetics, Immunoglobulin Class, and Specificity

Abstract A unique indirect plaque-forming cell (PFC) assay has been developed to assess the immune response to choleragen, a highly purified exo-enterotoxin derived from Vibrio cholerae cultures, at the cellular level. Spleen cells releasing anti-choleragen antibody were readily detectable with choleragen-sensitized sheep erythrocytes as “target” cells in a variation of the localized hemolysin in agar technique. Injection of 1-µg doses of the toxin into BALB/c mice was sufficient to stimulate large numbers of specific antibody PFC. Heat-treated choleragen preparations, i.e., procholeragenoid and choleragenoid, also induced a detectable immune response at 1-µg doses; however, the results indicate that the PFC response varied as a function of the dose and form of the cholera antigen used for immunization. Choleragen and procholeragenoid induced essentially similar immune responses and were more immunogenic than choleragenoid, although all immunogens stimulated IgM (19S) and IgG (7S) PFC. Peak IgM PFC responses were detected on days 6 and 7 whereas peak IgG PFC responses occurred 1 day later in all cases. A booster injection of choleragen (1 µg) increased the numbers of IgM and IgG PFC approximately 4- to 5-fold. IgA PFC were also detected after a booster injection. Specificity experiments revealed that the toxin and toxoid, but not a vibrio whole cell vaccine or lipopolysaccharide preparation, could inhibit the anti-choleragen PFC response.

Suppression of memory by passive immunization late in the primary response.

The acquisition of a capacity to respond well to sheep erythrocytes in the presence of anti-SRBC antibody was taken as an indication of the presence of immunological memory. By the use of passive immunization, both the primary IgG plaque-forming cell response and the establishment of memory were abolished, despite occurrence of a full peak IgM PFC response. Evidence for regarding the aquisition of memory and the IgM PFC and IgG PFC responses as three separate processes was presented. Antibody on day 3 of the response to 1.5 x 10(8) SRBC abolished formation of memory; this effect was less if passive immunization was further delayed and absent by day 10.