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Immune response were examined in 10-year-old boys just before and one month after tonsillectomy, and in young male adults tonsillectomized 10 years earlier. All the parameters studied were found to be quite normal.
In this paper, cell-mediated immunity (CMI) as evaluated by in vitro migration inhibition assays an in vivo delayed type skin reactions in experimental immune complex glomerulonephritis (ECGN) was studied as well as the effect of treatment with immunosuppressive drugs on these immune responses. In glomerulonephritic rats MIF production as well as delayed type skin reactions could be demonstrated directed against tubular brushborder antigen (Fx1A) containing immune complexes or to their constituents (FX1A or rabbit IgG). Treatment of the animals with immunosuppressive drugs during settled disease state (autologous phase) abolished these cellular immune reactions. However, neither the glomerular depositions of rat IgG associated with the autologous phase, nor the urinary excretion was influenced. When treatment of the animals was started simultaneously with the induction of the ECGN both cellular and humoral immune responses as well as proteinuria were affected. It was concluded that although in this glomerulonephritis model specific MIF response after specific stimulation in vitro as well as DTH reactions could be detected against immune complexes or their constituents, these immune reactions seem not to play important role in this ECGN in particular with respect to the proteinuria.
Immunization of mice with either soluble or particulate antigens induced a marked increase in peroxidase activity of spleen cell homogenates. Animals immunized with sheep erythrocytes showed maximum splenic peroxidase activity at 2 days. By the 4th day after immunization, when the hemolytic antibody plaque-forming cell response was maximal, peroxidase activity returned to normal levels. Increased splenic peroxidase activity also occurred in mice immunized with rabbit erythrocytes, as well as with rabbit serum or bovine serum albumin. No change in splenic peroxidase activity occurred in mice injected with syngeneic mouse erythrocytes or serum. Both glass-adherent spleen cell populations, morphologically consisting of 90 to 95% macrophages, as well as nonadherent cells, consisting of more than 90% lymphocytes by the same criteria, showed peroxidase activity. Immunization of mice with sheep erythrocytes resulted in an intracellular redistribution of the peroxidase activity among several distinct subcellular fractions prepared by differential centrifugation. Maximum redistribution occurred with granule-associated enzyme activity. A possible relationship between peroxidase activity with functional activity of lymphocytes and macrophages during humor immune responses seemed likely.
Antibody and cell-mediated immune responses were measured in rabbits immunized with live, UV inactivated herpes simplex virus or with a subunit vaccine containing envelope proteins. All the types of immunization procedures induced the production of antibody as well as a specific cellular immunity. Furthermore, the subunit vaccine was as effective as the immunization with live or UV inactivated virus to prevent death upon challenge with live HSV. Live HSV induced a transient unresponsiveness of both B and T cells to in vitro stimulation with various mitogens.
The immunizing abilities of alloantigens placed within the anterior chamber of the eye have been studied in inbred rats. Although intracameral inoculation of F1 hybrid lymphocytes into parental strain recipients elicited both cell- and antibody-mediated immunity, a delimited interval was identified postinoculation during which the systemic cell-mediated immune response was suppressed as indicated by prolonged acceptance of orthotopic skin allografts. The prompt appearance of hemagglutinating antibodies in the serum of immunized rats followed a time course which coincided with the suppression of cell-mediated immunity and suggested that the two events are casually related. Since exposure to allogeneic antigens on lymphoid cells via the anterior chamber elicits a transient suppression in cell-mediated immunity, where humoral immunity is preserved, the phenomenon resembles immune deviation.
We tested the ability of pepsin-extracted, highly purified M protein to induce type-specific immunity in experimental animals and humans. M protein was prepared from limited peptic digests of whole group A type 24 streptococci and was purified to chemical homogeneity as judged by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, quantitative amino acid analysis, and Edman degradation. For vaccination, the lyophilized M24 protein preparation (pep M24) was precipitated in aluminum hydroxide. When injected into laboratory animals, alum-precipitated pep M24 produced type-specific protective antibodies and was free of non-type-specific immunoreactivity. In man, skin tests with 1-microgram doses of pep M24 were negative in all 37 adults tested. 12 adult human volunteers received two-four subcutaneous injections of 100-200 micrograms of alum-precipitated pep M24 at intervals of at least 2 wk. The immune response to pep M24 was measured by a variety of assays designed to detect (a) type-specific humoral antibodies (opsonophagocytic, long chain, and mouse protection tests); (b) total humoral antibodies (complement fixation and enzyme-linked immunosorbent assay); (c) cellular immunity (skin tests); and (d) heart cross-reactive antibodies (immunofluorescence). Type-specific opsonic antibodies developed in 10 of the 12 vaccinees, and positive delayed-type skin tests developed in 11. Immune sera from two of the vaccinees were effective in mouse-protection tests against challenge with M24 but not M6 streptococci. None of the volunteers developed heart-reactive antibodies or antibodies to non-type-specific M protein antigens. Alum-precipitated pep M24 was well-tolerated in man, and no serious local or systemic reactions were observed. Thus, pep M24 induces type-specific, protective antibodies in doses that are well-tolerated in man.
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The primary and secondary immune response to the antigen bovine pancreatic alpha-chymotrypsin was investigated in inbred mice. It was found that strain differences in the immune response only became apparent after secondary immunization. The genetic control of the immune response was investigated in twelve different strains of mice, F1, F2 and F1 backcross hybrids, following secondary immunization. A continuous distribution for the mean antibody responsiveness was obtained. High responsiveness was associated with both the H-2 haplotype and three non-H-2 loci. Furthermore the F1 hybrids produced a greater quantitative antibody response to chymotrypsin than either of the corresponding parental strains.
Soluble tumor antigens were prepared from chemically-induced rat fibrosarcoma KMT-17 cells by various methods [Na-deoxycholate (DOC), 3 M-KCI extraction, and crude membrane preparations by mechanical disruption]. Soluble tumor antigens prepared by DOC extraction (DOC-STA) could be detected by a radioisotopic footpad assay (FPA) and they showed the strongest antigenic activity in KMT-17 immune rats. Anti-tumor immune responses in rats previously immunized with DOC-STA were measured by FPA, Winn assay, and transplantation resistance. Significant responses detected by the FPA and Winn assay were demonstrated in rats immunized with DOC-STA. However, rats previously immunized with DOC-STA showed a significant enhancement of tumor growth when challenged with KMT-17 cells. This enhancement was specific for the tumor line used. Normal rats which received adoptive transfer of thymus and spleen cells from rats immunized with DOC-STA produced specific enhancement of tumor growth as compared with non-treated rats. Administration of cyclophosphamide before immunization with DOC-STA abrogated the enhanced tumor growth in the host. These results suggest that immunization with soluble tumor antigens specifically enhanced tumor grwoth by the induction of immunosuppressor cells. Dissociation between the anti-tumor immunity detected by the FPA and Winn assay and the enhanced tumor growth detected by transplantation resistance in rats immunized with DOC-STA is discussed.
The immune response to the antigen bovine pancreatic alpha-chymotrypsin was investigated in ten recombinant strains of mice. Using a fixed antigen-percentage bound isotope technique, it was found that the quantity of antibody produced was related to the H-2 haplotype of the responding animal. A continuous distribution for the mean antibody responses was obtained for the ten strains of mice. High responsiveness was associated with the H-2 haplotype gamma2. The genetic control of the immune response to this immunogen was found to be both quantitative and qualitative.
Following immunization of mice with SRBC the kinetics of antibody synthesis by individual immunocompetent cells during the primary immune response were investigated. The diameter of the average hemolytic plaque using a modified Jerne plaquing technique, was taken to be an estimate of the antibody production by a single cell. We found an increase, followed by a decrease, of the average plaque diameter during the primary immune response. The increase of average plaque diameters is probably due to the raised rate of synthesis of antibody molecules. This increase can be accelerated by adjuvants. The decrease late in the primary immune response could be explained by an internally regulated switch from IgM to IgG antibody synthesis. The results are consistent with the mathematical approach of HELLWIG (1,2).
Since guinea pigs immunized with water-washed cell walls of Histoplasma capsulatum developed cellular immune responses detectable with cytoplasmic substances, attempts were made to determine whether cytoplasmic contamination of the walls was responsible for the induction of the immune response. Cell walls were treated by several procedures designed to remove possible contamination, namely, extraction with lipid solvents, incubation with proteolytic enzymes, and washing with sodium dodecyl sulfate, and each of the treated preparations was compared with water-washed walls for its ability to induce cellular responses demonstrable with cytoplasmic substances. For comparison, wall glycoprotein was also used as a test antigen. Immune responses were assessed by gross and histological examinations of skin test sites and by assays for the production of migration inhibition factor. A portion of the material inducing the response detectable with cytoplasmic substances was apparently removed or altered by each of the purifying procedures. The cellular immune responses to wall glycoprotein were also altered, however, indicating that more than the mere removal of cytoplasmic substances had occurred. On the basis of the data collected from each of the cellular assays involving wall glycoprotein as the test antigen, the hypothesis is proposed that sodium dodecyl sulfate altered or removed protein from the wall and thus augmented its ability to induce a more intense immediate-type hypersensitivity, whereas incubation with Pronase altered the walls in such a way as to shift the balance toward a more intense delayed-type hypersensitivity. The latter effect was probably due to the removal of carbohydrate from the wall by glucanase or to mannosidase contaminating the Pronase preparation.
The immune response to insulin, in both mouse and guinea pig, is under control of H-linked immune response genes. When immunized with either pork or beef insulin in CFA, both strain 2 and 13 guinea pigs respond by antigen-specific lymphocyte proliferation and synthesis of specific antibody. The specificities of the elicited antibodies and indistinguishable between these inbred strains. By constrast, strain 2 T cells recognized a distinct region of the A chain alpha loop consisting of amino acid residues 8, 9 and 10, while strain 13 T cells see an as yet undefined region of the B chain. H2b (A chain alpha loop responder) and H2d (B chain responder) mice similarly discriminate which areas of the molecule are recognized by their T lymphocytes. The function of the Ir gene in both the guinea pig and mouse appears to be an intramolecular selection of discrete regions within the antigen for recognition by the T cell. The data presented suggest that this function operates at the level of the macrophage.
The effects on the immune response of daily feeding of 30 mg of human serum albumin to rats have been studied. Feeding for periods of 17-20 days consistently resulted in a specific systemic hyporesponsiveness evident on subsequent parenteral immunogen challenge. Local secretory sites such as the major salivary glands were not made hyporesponsive as evidenced by the salivary antibody titres and the enumeration of glandular plaque-forming cells. The levels and classes of antibodies present in the secretions and sera were identified by passive haemagglutination, and a sensitive red-cell-linked antigen-antiglobulin reaction. By the use of radioimmunoassay and haemagglutination inhibition assays it was possible to quantitate the amount of antigen appearing in the circulation at varying times after feeding. It was shown in the use of oesophagectomised rats that absorption of small amounts of intact protein occurs from undefined sites in the oral cavity. Attempts were made to transfer the specific systemic hyporesponsiveness to syngeneic animals using spleen cell and serum transfers.
The immune responses of 26 Angus-Hereford fetuses and neonates to Escherichia coli O26:K60:NM were studied after bacterin or saline solution was injected (in utero) into the amniotic fluid. Calves were euthanatized at birth or were orally revaccinated; some were challenge exposed with live organisms. The hemolytic plaque assay was used to determine the presence of cells producing immunoglobulins M, G1, and G2 (IgM, IgG1, and IgG2) in 4 segments of the small intestine, mesenteric lymph nodes, and spleen. The passive hemagglutinin activity of intestinal washings was also determined. Anti-O26 passive hemagglutinin activity in the intestinal washings of principal calves was greater than in that of control calves, but in a given segment of the small intestine, usually this activity was relatively small and less consistent than the plaque-forming response. Greater numbers of plaque-forming cells were observed in the small intestine of 14 of the 15 principal calves when compared with the control calves tested.
The immune response to beta-galactosidase (beta-D-galactoside galactohydrolase; EC 3.2.1.23)is characterized by a wave of early help followed by a wave of suppression to a subsequent in vitro challenge with galactosidase-fluorescein. A cyanogen bromide peptide of beta-galactosidase, CB2, mimics the suppression seen with the enzyme. It is time dependent, carrier specific, and anti-theta sensitive; however, this suppression is not preceded by a wave of help. It is possible that CB2 cannot stimulate helpers, and is only able to activate suppressor cells. These data indicate that one small region of an antigen, capable of activating suppressors, can nullify the positive effect induced in helper T cells reactive with other epitopes on beta-galactosidase. Key determinants on macromolecules may in this way be influential in regulating the immune response to the entire antigen molecule.
The effects of the emulsion of quinonyl acids (QS-n, ES-n, KS-n) and related compounds (QSA-n) in Freund's incomplete adjuvant on the humoral immune response to bacterial alpha-amylase were assayed, and their structure-adjuvant activity relationships were discussed. All the quinonyl acids tested (500 microgram/mouse) enhanced the humoral immune response two to seven times as much as that of the control group, five weeks after immunization. 3'-Methyl and 2', 3'-double bond in the carboxy side chains of ubiquinone metabolites (Q acid-I, -II) were not essential for the adjuvant activity. The conversion of methoxyls on the quinone ring into methyls, and that of benzoquinone into phenol also did not affect the activity, but the activity seemed to depend on the carbon number of the carboxy side chain, and the prominent adjuvant activity was observed in the carboxylates having the carboxyalkyl chain of five to seven carbons. High doses (1 or 5 mg/mouse) of ubiquinone-7 and -2 enhanced the humoral immune response two to three times as much as that of the control group, and quinonyl alcohols (QSA-n) enhanced that with low dose (500 microgram/mouse).
Spleen cells of dinitrophenyl keyhole limpet hemocyanin (DNPKLH) primed and boosted mice produced a nonantigen-specific helper factor upon in vitro challenge with DNPKLH. This helper factor displays all of the biological characteristics so far described for TRF produced by allogeneic or Concanavalin A stimulation of mouse spleen cells. It restores the primary anti-SRBC response in nude spleen cultures following the same kinetics of action as T-cell-replacing factor (TRF). Conversely, TRF restores the primary in vitro immune response of nude spleen cultures to DNPKLH. TRF also restores the secondary anti-hapten IgG response of T-cell-deprived spleen cell cultures derived from DNPKLH primed and boosted mice. Here the need for carrier specificity is fully overcome. The data therefore suggest that TRF, as a nonantigen-specific maturation signal, is involved in the primary and secondary immune responses to both particulate and soluble antigens.