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F Nagase

Publications and source records attributed to F Nagase.

At least 73 records · Page 4Linked to original sources
PubMed1983

Studies on the immune response in chickens. IV. Generation of hapten-specific memory and absence of increase in carrier-specific helper memory in antibody response to sheep red blood cell antigen and its hapten-conjugate.

The role of carrier recognition in the hapten-specific antibody response of chickens to hapten (TNP) conjugate of sheep red blood cells (SRBC) was studied. The anti-TNP antibody response to the challenge with either TNP-SRBC or DNP conjugate of Salmonella enteritidis (DNP-Sal) of chickens previously primed with TNP-SRBC was definitely higher than that of unprimed chickens. Injection of TNP-chicken red blood cells, which did not provoke any significant primary anti-TNP response, also induced the memory for secondary anti-TNP response to the challenge with TNP-SRBC or DNP-Sal. The TNP-specific memory generated by stimulation with TNP-SRBC was adoptively transferable by spleen cells into cyclophosphamide (CY)-treated X-irradiated syngeneic recipients. On the other hand, the SRBC-specific memory for augmentation of anti-TNP response to the challenge with TNP-SRBC was never detected in chickens previously primed with either any of a wide range of doses (10(4)-10(8)) of SRBC, solubilized SRBC or SRBC fixed with formaldehyde, nor in CY-treated X-irradiated chickens receiving SRBC-primed spleen cells. The anti-TNP response of chickens to the challenge with TNP-SRBC was rather suppressed by the SRBC preimmunization. The passively administered anti-SRBC chicken serum also suppressed the response to TNP-SRBC. The carrier-specific suppressor activity generated by SRBC stimulation was not adoptively transferable by spleen cells. It is suggested from these results that the mechanism of amplification of the anti-hapten antibody response of chickens to hapten-SRBC conjugate is primarily mediated by the hapten-recognition, and carrier-recognition is more important for suppression rather than for amplification of the anti-hapten response, although the inductive mechanism for anti-hapten response itself should somehow involve the carrier recognition.

Animals↗
PubMed1983

Intact and subcellular form of thymocytes of rats are exceptionally immunogenic in mice for inducing anti-Thy-1 T cell-independent class 2 antibody responses.

Results of the present study show that the primary anti-Thy-1.1 antibody response to rat antigen in Thy-1.2 mice is induced exclusively by thymocyte antigen. Thy-1 antigens of brain and bone marrow, which expressed much Thy-1 antigen, were poorly immunogenic if at all. Brain Thy-1 antigen considerably inhibited the immunogenicity of thymocyte Thy-1. Moreover, we found that subcellular form of thymocytes induce as high antibody responses as intact thymocytes do. The subcellular thymocyte Thy-1 antigen behaved as TI-2 antigen, inducing a good response in athymic nude mice but not in CBA/N mice with a B cell defect. The significance of these findings is discussed in relation to the possible physiological activity of Thy-1 or Thy-1-linked molecules on thymocytes specifically mediating lymphocyte differentiation.

Animals↗
PubMed1983

Control of T-cell-dependent antibody responses of mice to rat antigens by donor cell types.

Administration of rat red blood cells (RBC) into mice induced a rat antigen-specific T-cell-dependent primary antibody response that was detected by a plaque assay using rat RBC as a target. This response was not induced by rat thymocytes or rat spleen cells that should share rat-specific antigens with rat RBC. We then demonstrated that rat spleen cells but not rat thymocytes, which were administered with rat RBC, partially inhibit the action of rat RBC for induction of the anti-rat response. This inhibition required live donor FcR+ cells, and seemed to be specific to rat antigens common to RBC and spleen cells. The findings supported the idea that the control by donor cell types, which was originally shown to work for T-cell-independent antibody response [3,5], should be effective for T-cell-dependent response beyond the species barrier.

Animals↗
PubMed1983

Evidence for the erythrocyte as the principal antigenic cell type that triggers primary IgM antibody responses to H-2D alloantigens.

Antigenic requirements for the induction of T cell-independent primary splenic IgM antibody responses (plaque-forming cell responses) to H-2Dd alloantigens were studied. Results show that some functional activity or structural property of the donor cells is required for immunogenicity, because antigens are not active in subcellular forms. An unexpected finding was that allogeneic red blood cells were exceptionally highly immunogenic, and any lymphoid tissues including purified macrophages and tumor cell lines that were not contaminated with red blood cells were virtually nonimmunogenic. The definite role of red blood cells in donor tissues as immunogens was confirmed by water or ammonium chloride treatment that abolished immunogenicity, as well as by phenotyping of the immunogenic cells with antisera. Thus immunogenic cells were positive for erythrocyte-specific and H-2D antigens and negative for Thy-1, Ig, and NK-1. The possible roles of erythrocytes in induction and regulation of transplantation immunity and in B cell activation in general are discussed.

Animals↗
PubMed1982

Control of primary IgM antibody responses to H-2 alloantigens by antigen-bearing live B lymphocytes.

Alloantigen-bearing (H-2d+) peripheral red blood cells, but not red cell-depleted H-2d+ spleen cells, induce primary IgM anti-H-2d plaque-forming cell responses. In this study it is reported that the primary antibody responses to H-2d+ peripheral red blood cells can be markedly suppressed by a subpopulation of H-2d+ spleen cells when they are injected simultaneously or a few days before injection of red blood cells. This suppression was antigen (H-2d)-specific, did not depend on T cells of either the donor or the recipient, and strictly required live donor cells. An energy-dependent action of the donor cell cortex and some proliferation of donor cells in the recipient seemed to be involved in the mechanism of suppression. The donor-suppressor cell type was largely present in the spleen but not in the bone marrow and thymus, and was present in the spleen of athymic nude mice. The suppressor cells displayed the properties of B lymphocytes: they adhered to the nylon wool but not to glass, were of relatively low density (rho less than 1.09), and were surface Ig+, Ia+, Fc receptor-positive but Thy-1-. H-2d+ suppressor-donor B lymphocytes might directly signal to antigen-specific recipient B cells competing with the signal provided by H-2d+ red blood cells for the B cell activation.

Animals↗
PubMed1982

The donor cell type controls anti-hapten (fluorescein isothiocyanate) primary antibody response to hapten-modified syngeneic cells.

Hapten (fluorescein isothiocyanate, FITC)-sensitized syngeneic red blood cells (FITC-RBC) are exceptionally active for induction of anti-hapten primary antibody response, and FITC-modified syngeneic spleen cells depleted of RBC (FITC-SSC) are not immunogenic [4]. The present study has demonstrated that FITC-SSC injected simultaneously with FITC-RBC inhibit partially the anti-FITC response to the latter. Either the immunogenicity of FITC-RBC or the response-inhibiting activity of FITC-SSC was increased as the concentration of hapten-sensitizing cells was raised from 0.005 mg/ml to 2 mg/ml. The inhibition of anti-FITC response by FITC-SSC strictly required live donor cells, but was not dependent on T-cell activity of either the donor or recipient. Neither FITC-thymocytes nor the FITC-T-cell-rich fraction of SSC showed a definite activity for inhibition, whereas the FITC-B-cell-rich fraction of SSC acted very effectively. These results suggest that the primary anti-hapten antibody response to hapten-modified syngeneic cells is primarily controlled by antigen-bearing live donor cells of different cell types.

Animals↗
PubMed1982

Alterations in the immunogenic properties of sheep erythrocytes by sonic disruption.

A solubilized sheep red blood cell (SRBC) antigen (supernatant fraction obtained by centrifuging 10(7)-2 x 108 sonicated SRBC at 6 x 10(4) g for 30 min [Sup-SRBC]), whose ability to inhibit anti-SRBC plaque formation was 70% of that of the original sonicated SRBC, was unable to elicit a detectable antibody response in either unprimed or SRBC-primed mice. However, Sup-SRBC as well as intact SRBC antigens generated memory for the secondary response, which was transferable to irradiated syngeneic recipients by injection of immune spleen cells. The memory generated by Sup-SRBC involved helper memory for anti-trinitrophenyl group (TNP) response to challenge with TNP-conjugated SRBC. Increase in the helper T cell memory in the spleens of Sup-SRBC-primed mice was also demonstrated by an in vitro culture experiment and by an adoptive cell transfer experiment. In contrast, no detectable B cell memory was generated by Sup-SRBC. Repeated stimulation with Sup-SRBC never induced significant antibody response but reduced the level of memory. A single injection of a low dose (10(6)) of SRBC also failed to induce a definite primary antibody response generating memory for the secondary response. However, repeated stimulation with this dose of SRBC induced a high antibody response and generated good memory. From these results it is suggested that the intact structure of SRBC is required for the activation of B cells, but is not necessary for the stimulation of T cells.

Animals↗
PubMed1982

Further studies of the polysaccharide of Klebsiella pneumoniae possessing strong adjuvanticity. III. Augmentation of the antibody response to subcutaneously injected sheep red blood cells by the adjuvant polysaccharide.

The adjuvant action of the O3 antigen of Klebsiella (KO3) on the antibody response to sheep red blood cells (SRBC) was elucidated by injecting both KO3 and SRBC subcutaneously at the right inguinal region of SMA mice. We demonstrated that KO3 exhibits a novel ability to augment anti-SRBC plaque-forming cell responses in both the local lymph node and the spleen at a relatively late stage of immunization. Escherichia coli lipopolysaccharide, dextran sulfate and concanavalin A showed such an action only minimally. In parallel with the development of the adjuvant action, KO3 definitely activated B cells in the local lymph node polyclonally for either IgM or IgG synthesis, suggesting that the mechanism of the adjuvant action includes direct stimulation of B cells by KO3 at the late stage. Neither increase in trapping of lymphocytes in the local lymph node nor change in tissue distribution of antigen was shown to be primarily involved in the mechanism of the adjuvant action.

Adjuvants, Immunologic↗
PubMed1981

Primary antibody responses to hapten-modified syngeneic cells: exceptional immunogenicity of erythrocytes.

Intravenous injection of fluorescein isothiocyanate-modified syngeneic spleen cells (FITC-SSC) into mice induced T cell-independent, anti-hapten plaque-forming cell responses. In contrast to the high immunogenicity of FITC-coupled SSC or bone marrow cells, thymus, lymph node or peritoneal exudate cells were poorly immunogenic. Further analysis showed that FITC-syngeneic peripheral blood red cells were as immunogenic as FITC-SSC containing a similar number of red cells. The immunogenicity of the red cells was confirmed by treatment of FITC-SSC with 0.83% ammonium chloride before sensitization with FITC. This procedure almost totally abolished the immunogenicity regardless of the concentration of hapten with which they were sensitized. In addition, heat treatment or fixation with glutaraldehyde destroyed the immunogenicity of FITC-SSC.

Ammonium Chloride↗
PubMed1981

Further Studies of the polysaccharide of Klebsiella pneumoniae possessing strong adjuvanticity. I. Production of the adjuvant polysaccharide by noncapsulated mutant.

In culture fluid, Klebsiella pneumoniae type 1 Kasuya strain produces polysaccharide exhibiting a strong adjuvant effect. The active substance responsible for the strong adjuvant effect of the polysaccharide isn ot its acidic polysaccharide fraction (the type-specific capsular antigen) but the neutral polysaccharide fraction. In the present study, a mutant which did not produce the type-specific capsular polysaccharide was isolated from ultraviolet-irradiated cells of K. pneumoniae type 1 Kasuya strain which had been labeled with leucine-requiring marker by selecting unagglutinable cells with the antiserum to he type-specific capsular polysaccharide. Serological tests showed that the type-specific acidic capsular polysaccharide was present neither on the cells surface nor in the culture fluid of the mutant. Electron microscopically, the mutant did not possess any capsular material. On the other hand, nearly an equal amount of neutral polysaccharide antigen as produced in culture fluids of the noncapsulated mutant polysaccharide antigen was produced in culture fluids of te noncapsulated mutant and the parent strain. The neutral polysaccharide antigen produced by the noncapsulated mutant exhibited the same degree of strong adjuvant effect on antibody response to bovine gammaglobulin in mice as that produced by the parent strain. The relationship between the neutral polysaccharide antigen in culture fluid and the O antigen of K. pneumoniae was discussed.

Adjuvants, Immunologic↗
PubMed1980

Formation of mononuclear phagocyte (macrophage) colonies by mouse spleen cells in liquid culture. I. Kinetics of appearance of colonies and characterization of macrophage colony-forming cells.

When spleen cells of the adult mouse were tested for the formation of mononuclear phagocyte (macrophage) colonies by the liquid culture technique with an incubation period of 7--8 days, about 100 macrophage colonies were produced from 1 X 10(6) cells. The number of macrophage colonies appearing after 2 days of incubation was small, but thereafter increased progressively up to at least 8 days. In the later stages of incubation (after day 6) large colonies consisting of more than 100 cells appeared. Macrophage colonies in the early stages consisted almost solely of macrophages. On day 6 significant numbers of small round mononuclear cells with no detectable phagocytic activity were seen in the center of large colonies, and by day 8 marked crowding of these cells had occurred. The peripheral region of the large colonies consisted mainly of macrophages and the intermediate region of middle-sized round or slightly stretched cells with weak phagocytic activity. Approximately two-thirds of the colony-forming cells still remained after glass-adherent cells were removed from the spleen cells by passing over a glass-bead column. In cultures of glass-nonadherent cells macrophage colonies were not generated in the early stage. The number of colony-forming cells did not change significantly even after actively phagocytic cells were rigorously removed from the spleen cells. In addition, no macrophage colonies were generated in cultures of spleen cells treated with mitomycin C.

Animals↗
PubMed1980

Interferon and cytotoxic factor (cytotoxin) released in the blood of mice infected with Mycobacterium bovis BCG. III. Interferon and cytotoxin induced by the specific antigen as compared with those induced by bacterial lipopolysaccharide.

The time course of development and decline of the ability of BCG-infected mice to produce interferon in the serum in response to the intravenous infection of purified protein derivative of tuberculin (PPD) was very similar to that of their systemic hypersensitivity to PPD. A cytotoxic factor (cytotoxin) was produced in parallel with interferon in the serum of BCG-infected mice after stimulation with PPD. The duration of the period in which cytotoxin-production responsiveness to PPD was definitely detectable was much shorter than that for interferon-production responsiveness although the periods for the maximum production of interferon and cytotoxin coincided. The kinetics of release of interferon in the serum of BCG-infected mice after stimulation with PPD did not parallel that of release of cytotoxin. The four kinds of activities, interferons and cytotoxins induced by PPD and lipopolysaccharide (LPS) in the serum of BCG-infected mice, were compared for their stability to heating at 56 C and to treatment at pH 2. The kinetics of inactivation of these four activities differed significantly, when the serum was either heated at 56 C or treated at pH 2. Interferon produced in response to LPS could be neutralized by anti-L cell(NDV) interferon rabbit serum as easily as L cell (NDV) interferon, 16 times as much antiserum was required to neutralize the same amount of interferon in response to PPD, but cytotoxins induced by PPD and LPS were not neutralized at all by the antiserum. From these findings it is thought likely that interferons and cytotoxins induced by PPD and LPS in the serum of BCG-infected mice are different substances, although the antigenic relationship between cytotoxins induced by PPD and LPS remains unknown.

Animals↗
PubMed1979

Studies on the immune response in chickens. III. Effect of substitution of carrier on elicitation of anti-hapten antibody responses and generation of hapten-specific memory.

The role of carrier in both elicitation of anti-hapten antibody responses and generation of hapten-specific memory in chickens were studied using dinitrophenyl (DNP) conjugate of T-independent antigen carrier (DNP--Ficoll), that of isologous serum protein DNP--chicken serum albumin (CSA), and heavily conjugated DNP--bovine gammaglobulin (BGG). All of these DNP--conjugates could generate DNP specific memory as markedly as moderately conjugated DNP--BGG. Both DNP--Ficoll and DNP--CSA hardly elicited the primary and secondary anti-DNP antibody responses. Heavily conjugated DNP--BGG did not elicit a significant primary anti-DNP response as moderately conjugated DNP--BGG. It is suggested therefore that, when chickens are stimulated with hapten-carrier conjugates, hapten-specific memory is generated independently of T-cell function, but the elicitation of both the primary and secondary anti-hapten antibody responses is somehow relevant to T-cell function, although the T-cell dependence is less marked in the secondary than in the primary response.

Animals↗