Number Of Antigen-binding Cells Research Articles

The immune system response to antigen in cold- and warm-adapted rats

In rat experiments, it was shown that long-term adaptation to cold modified the response pattern of the immune system to antigen stimulus by variously changing the different components of the response. There was a considerable decrease in the number of antigen-binding cells in spleen and peritoneal exudate and also a marked decrease in general antibodies in blood. Conversely, the number of antibody-forming cells in spleen increased twofold. The shift in the thermal conditions after immunization caused changes in the immune response. After the placement of cold-adapted animals to the warm environments the number of antigen binds and antibody-forming cells in spleen, as well as hemagglutinin titers in serum normalized, became indistinguishable from those in the warm-adapted control group. The placement from warm to cold after immunization of warm-adapted rats also produced considerable shifts in parameters of the immune response. However, these shifts were not entirely consistent with those observed for long-term adapted to cold. The obtained data evidence that the thermal factor of the environment is of major importance to the function of immunocompetent cells.

Effects on N-Methyl-N-Nitrosourea on Carrier-Primed Anti-Hapten Responses in Xenopus Laevis

Young adult Xenopus laevis were treated with N-methyl-N-nitrosourea at doses which temporarily or permanently remove the thymic cortex and suppress allograft immune competence. Their ability to mount a carrier-primed, helper T cell-mediated, hapten-specific response was tested in terms of numbers of antigen binding cells in the spleen. Animals which had retained skin allografts for more than 300 days lacked helper activity, while those which had eventually rejected their allografts were able to mount an anti-hapten response. All groups of Xenopus exposed to the carcinogen rejected skin xenografts after the same time as untreated control animals.

Physiological regulation of antigen binding to T cells: role of a soluble macrophage factor and of interferon.

A soluble product of macrophages (MF) and mouse viral interferon (IF) increase both major histocompatibility antigenic determinants and the number of antigen-binding cells in nonstimulated T cell-enriched mouse lymphocyte cultures. MF increases Ia and not H-2 antigens; IF increases H-2 but not Ia antigens. The increased antigen binding due to MF can be inhibited by anti-Ia but not by anti-H-2 sera, whereas IF-induced binding is sensitive to anti-H-2 but not to anti-Ia sera. The specificity of IF- or MF-induced binding of branched synthetic polypeptides by T cells is different from that of B cells and similar to the specificity of the Ir gene regulation. MF increases antigen binding only in Ir high-responder animals. The IF-induced antigen binding is not dependent on the Ir genotype. MF-reactive cells express the Ly-1 marker, and the IF-reactive antigen binders express the Ly-2 phenotype. It is suggested that MF and IF are physiological mediators of antigen binding by T cells.

Influence of different antigen doses on number and properties of antigen binding cells

The number of antigen binding cells, as revealed by capping experiments, is strongly influenced by the concentration of antigen used. At high concentrations of antigen an additional population of cells of the size of lymphocytes can be detected, which is not stained after incubation with low doses of antigen. These cells bear immunoglobulin on their surface and can be removed from the spleen by carbonyl iron treatment.

Polyfunctional antigen-binding specificity in hapten-carrier responses of the newt, Triturus viridescens.

Carrier specific enhancement of an anti-hapten response has been reported for spleen cells of the newt, Triturus viridescens (1). The response was monitored by using immunocytoadherence (ICA). Pooled chicken or toad (Bufo marinus) erythrocytes (CRBC or TRBC) were conjugated with 2, 4, 6 trinitrophenyl (TNP) as previously described. TNP-TRBC were injected intraperitoneally (i.p.) and after 8 days sensitized spleen cells from 4 adult newts were mechanically dissociated, pooled, washed, counted and incubated 12–16 hours at 4°C with either horse erythrocytes (HRBC) or TNP-HRBC. Spleen cells previously sensitized to test immunogens will bind them on their surface. After the incubation, the numbers of antigen binding cells (ABC) in each incubation mixture were counted in hemacytometer chambers. In the absence of carrier immunization or with immunization by injection of an erythrocyte species other than the one used as carrier, a consistently small proportion of the spleen cells bound either antigen. This low degree of binding, which exceeded that found when no prior immunization was effected, served as a measure of cross reactivity between the two erythrocyte species used. However, when the newt spleen cells had been sensitized with the carrier species of erythrocytes within 4 days prior to hapten presentation, a substantial enhancement in the number of cells binding TNP-HRBC over those binding HRBC was observed. The number of cells binding due to cross reactivity between the carrier and HRBC, which was itself enhanced by immunization, can be subtracted from the average number of TNP-HRBC ABC in order to arrive at the number of TNP specific ABC. That these were indeed TNP specific was shown by pre-incubating the sensitized spleen cells with TNP-human serum albumin (HSA) prior to performing the binding assay. Only TNP-HRBC ABC were blocked, those remaining reflecting the degree of cross reactivity with HRBC. Because similar results obtained with other animals (e.g. the rodent) were shown to reflect cell cooperation between carrier specific “helper” and antibody producing cell (APC) subpopulations (2, 3, 4), it was suggested the cell cooperation was also required for hapten responses in the newt. This assumption was strengthened by further studies (5) which showed that, as in the rodent (6), low immunogen doses (0.0025% RBC) enhance “helper” activity, even when they do not stimulate antibody synthesis. It was found that low and high immunogen dose-initiated antigen binding responses exhibit very different kinetics. Low dosages stimulate maximum ABC activity by 2 days, while high doses generated a much higher number of ABC, but this activity did not reach a maximum until 8 days post-primary challenge. While we cannot yet be certain, this difference is at least consistent with the hypothesis that two populations of spleen cells can be visualized by ICA and that they are involved in antihapten responses in the newt.KeywordsSpleen CellAntigen BindingAntibody Produce CellAdult NewtPrior ImmunizationThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Immunogenicity, Tolerogenicity, and Mitogenicity of Lipopolysaccharides

Lipopolysaccharide (LPS) is an immunogen that often induces synthesis of IgM only, and these antibodies exhibit regular cyclical fluctuations due to an antibodymediated feed-back regulation. LPS can induce high-dose immunologic tolerance; however, tolerant animals have an increased number of antigen-binding cells, even though the number of antibody-producing cells is depressed. Tolerance to LPS is rapidly broken by incubation of lymphocytes in tissue culture for 24 hr or by adoptive transfer of tolerant cells to irradiated hosts, suggesting the existence of cells tolerant to this antigen. LPS is also a mitogen capable of activating DNA synthesis in bone-marrow (B) cells but not in thymus (T) cells. LPS-activated B cells secrete IgM antibodies against a variety of antigens. It is most likely that LPSactivated B lymphocytes differentiate into cells that produce antibody at a high rate and that express their genetically determined antibody specificity. When LPS is coated onto T-cell-dependent, heterologous red cells, the latter become T-cellindependent, presumably because of the mitogenic properties of LPS. LPS can substitute for both T cells and macrophages in the induction of a primary immune response in vitro, suggesting that LPS acts directly on B cells and that at least one function of the helper is immunologically nonspecific.

Fate of antigen-binding cells in unresponsive and immune mice.

Antigen-binding cells (ABC) to the antigen human gamma globulin (HGG) were quantitated in lymphoid tissues of A/J mice at various times after the injection of deaggregated HGG (tolerogen), aggregated HGG (immunogen), or saline. The reaction of lymphoid cells with highly labeled HGG was specific to that antigen since binding could be inhibited by excess unlabeled HGG, but not by unrelated non-cross-reacting proteins. Compared with normal mice, there was a marked decrease in the numbers of ABC in the spleens of unresponsive animals evident as early as 12 h after the injection of tolerogen. A marked increase in ABC was observed in the spleens of immunogen-injected mice, beginning at 24 h and reaching a peak at 3 days. In bone marrow, no difference in the number of ABC was found among the three experimental groups until day 20, when a reduction in ABC was observed only in tolerogen-injected mice. No quantitative difference in the thymuses in the experimental groups could be determined because of the paucity of ABC displayed by normal thymus cells.