研究者詳細 - 竹内　勤

論文 - 竹内　勤

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EXPRESSION OF CELL-ADHESION MOLECULES IN THE SALIVARY AND LACRIMAL GLANDS OF SJOGRENS-SYNDROME

竹内勤

Journal of Clinical Laboratory Analysis 7 （ 3 ） 180 - 187 1993年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0887-8013

The presence of anti-protein A antibodies in patients with rheumatoid arthritis

Takeuchi T., Hosono O., Koide J., Amano K., Sekine H., Abe T.

Scandinavian Journal of Immunology 33 （ 5 ） 585 - 592 1991年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0300-9475

Sixteen patients with rheumatoid arthritis (RA) were examined for the presence of anti-protein A antibodies. The F(ab')₂ preparations from five RA patients showed significant binding to IgG-free protein A on ELISA. The protein A binding was further examined by immunoblotting. The F(ab')₂ preparations of high protein A-binding protein gave a specific reaction with IgG-free protein A on nitrocellulose paper. This demonstrates the presence of anti-protein A antibodies in patients with RA. Those RA patients with anti-protein A antibodies had more active disease as judged by the Lansbury's activity index. The level of serum rheumatoid factor (RAHA) was significantly higher in patients with anti-protein A antibodies than in those without anti-protein A antibodies.

Thrombotic thrombocytopenic purpura in two patients with systemic lupus erythematosus

Itoh Yoshihiro, Sekine Hiromi, Hosono Osamu, Takeuchi Tsutomu, Koide Jun, Takano Makoto, Abe Tohru

Clinical Immunology and Immunopathology 57 （ 1 ） 125 - 136 1990年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0090-1229

Thrombotic thrombocytopenic purpura (TTP) is a clinical syndrome of unknown etiology and has a high mortality rate due to disseminated platelet thrombi. However, the mechanism of platelet agglutination is not understood. Although an immunological mechanism has been suggested as the basis for the pathogenesis of TTP, any possible immunemediated etiology remains unclear. The association of TTP with systemic lupus erythematosus (SLE) affords a unique opportunity to study such possibilities, because SLE is a prototype of autoimmune disease. This report describes two patients with SLE who developed TTP. The development of anti-platelet antibodies is one possible immunological mechanism for platelet agglutination in patients with SLE complicated by TTP. More importantly, patient J.Y., who had anti-platelet antibodies, responded dramatically to high doses of prednisolone. © 1990.

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CCA [N-(2-carboxyphenyl)-4-Chloroanthranilic acid disodium salt], a newly developed immunomodulating drug, suppresses T-cell activation by acting on macrophages

Takeuchi Tsutomu, Koide Jun, Hosono Osamu, Takano Makoto, Abe Tohru

Inflammation 13 （ 2 ） 125 - 135 1989年04月

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0360-3997

The cellular mechanism of action of a newly developed drug, CCA, N-(2-carboxyphenyl)-4-chloroanthranilic acid disodium salt, on PHA-, autologous mixed lymphocyte reaction (AMLR)-, and phorbol myristate acetate (PMA)-stimulated T-cell proliferation was investigated. Addition of 50 μg of CCA per milliliter suppressed PHA- and AMLR-stimulaled T-cell proliferation. In contrast. CCA failed to suppress PMA-stimulated macrophage-depleted T-cell proliferation. After treatment of T cells or macrophages with CCA for 12 h, recombined T cells and macrophages were stimulated with phytohemagglutinin. [³H]Thymidine incorporation by T cells was suppressed when macrophages but not T cells were treated with CCA. These results indicate that CCA suppresses T-cell proliferation by acting on macrophages. The mechanism involved in this suppression of CCA was due to the loss of Ia antigen on macrophages and the loss of interleukin-1 (IL-1) secretion from macrophages. © 1989 Plenum Publishing Corporation.

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Functional characterization of the CD45R (2H4) molecule on CD8 (T8) cells in the autologous mixed lymphocyte reaction system

Takeuchi T., Rudd C. E., Tanaka S., Rothstein D. M., Schlossman S. F., Morimoto C.

European Journal of Immunology 19 （ 4 ） 747 - 755 1989年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0014-2980

In the present study, we have investigated the molecular basis for the immunoregulatory function of CD8 cells after autologous mixed lymphocyte reaction (AMLR) activation. We demonstrated that the CD8⁺CD45R⁺, but not the CD8⁺CD45R^- subset of cells effected suppression following AMLR activation. In contrast, cytotoxic activity against alloantigens resided in both the CD8⁺CD45R⁺ and CD8⁺CD45R^- subsets of cells. Biochemical analysis showed that on CD8 cells, the 220-kDa isoform of the LCA/T200 antigen family was better represented than the 200-kDa isoform, when compared to CD4 cells. The density of the CD45R antigen increased on CD8 cells following activation in AMLR and treatment of AMLR-activated CD8 cells with either anti-CD45R antibody or anti-CD3 antibody abolished the suppressor function of these cells. In contrast, treatment of AMLR-activated CD4 cells with anti-CD45R, but not anti-CD3 antibody, abolished the suppressor/inducer function of these cells. The results suggest that the CD45R antigen as well as CD3 T cell receptor complex have an important role in the suppressor function of AMLR-activated CD8 cells.

Amplification of suppressor inducer pathway with monoclonal antibody, anti-2H4, identifying a novel epitope of the common leukocyte antigen/T200 antigen

Takeuchi Tsutomu, Rudd Christopher E., Tedder Thomas F., Schlossman Stuart F., Morimoto Chikao

Cellular Immunology 118 （ 1 ） 68 - 84 1989年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0008-8749

The 2H4 antigen, comprised of a 200 220-kDa glycoprotein of the leukocyte common antigen (LCA) family, is expressed on a suppressor inducer, but not a helper inducer subset of T4 cells. Earlier studies have demonstrated that the T4+2H4+ subset of cells maximally responded to the AMLR and this molecule had an important role in generated suppressor signals in AMLR/ Con A-activated T cell systems. In the present study, we examined the effect of a series of monoclonal antibodies including anti-2H4 antibody on the initial activation of T4 cells in response to self-Ia antigens. We found that the addition of anti-2H4 antibody resulted in an augmentation of the proliferative response of T4 cells in AMLR, whereas other antibodies reactive with LCA/ T200 antigens lacked this ability. Furthermore, anti-2H4 antibody enhanced both IL-2 production and IL-2R expression in this AMLR system. This enhancing effect was inhibited by anti-T3 antibody. Moreover, the suppressor inducer function of AMLR T4 cells was enhanced with anti-2H4 antibody by increasing the number of 2H4+ cells with high antigen density. Taken together, these results suggest that the 2H4 antigen may serve as an accessory structure for enhancing the activation of the T4+2H4+ suppressor inducer subset at initiation of cell triggering. © 1989.

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Cellular regulation of anti-nRNP antibody synthesis is different from that of anti-DNA antibody synthesis in patients with systemic lupus erythematosus

Hosono O., Takeuchi T., Koide J., Takano M., Abe T.

Rheumatology International 8 （ 4 ） 177 - 183 1988年08月

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0172-8172

The cellular regulation of anti-nuclear ribonucleoprotein (nRNP) antibody synthesis in patients with systemic lupus erythematosus (SLE) was examined and compared with that of anti-double-stranded DNA (dsDNA) antibodies. In vitro antibody production by lymphocytes from SLE patients with antibodies to either dsDNA or nRNP alone was measured using dsDNA-specific and nRNP-specific solid-phase radioimmunoassays (RIA). Lymphocytes of SLE patients with only anti-dsDNA antibodies and normal individuals failed to synthesize anti-nRNP antibody with or without nRNP stimulation. In contrast, lymphocytes from SLE patients with anti-nRNP antibody alone in their sera synthesized in vitro a large amount of anti-nRNP antibody with or without nRNP stimulation. Experiments with reconstituted autologous lymphocytes indicated that B cells and T cells were required for anti-nRNP antibody synthesis. As expected, helper function for antibody synthesis by autologous B cells resided in the T4-cell population and suppressor function in the T8-cell population. T8 cells from SLE patients with anti-nRNP antibody alone suppressed anti-nRNP antibody synthesis by autologous B cells irrespective of clinical activity. This is in contrast to anti-dsDNA antibody production, which was not suppressed by autologous T8 cells. These results indicate that the cellular regulation of anti-nRNP antibody synthesis in SLE is different from that of anti-dsDNA antibody syntheis. Increased anti-nRNP antibody synthesis may be due to increased T4-helper cell function rather than defective T8-suppressor function. © 1988 Springer-Verlag.

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CD11 molecule defines two types of suppressor cells within the T8⁺ population

Takeuchi Tsutomu, DiMaggio Marjorie, Levine Herbert, Schlossman Stuart F., Morimoto Chikao

Cellular Immunology 111 （ 2 ） 398 - 409 1988年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0008-8749

It has been shown that T8⁺ cells are comprised of functionally heterogeneous subpopulations such as suppressor, cytotoxic, and NK cells. In this report, we attempted to delineate the functional heterogeneity of T8 cells defined by anti-CD11 antibody (anti-Mol). Although allospecific cytotoxic activity was restricted to the T8⁺Mol^- subset, suppression of PWM IgG synthesis could be elicited in both the T8⁺Mol⁺ and the T8⁺Mol^- subset of cells. However, the mechanism of suppression was different in these two subsets. Suppression by the T8⁺Mol^- subset of cells required the interaction with the T4⁺2H4⁺ suppressor inducer cells, whereas the T8⁺Mol⁺ subset of cells could suppress in the absence of the suppressor inducer cells. Moreover, recombinant interleukin-2 alone could augment this suppression by the T8⁺Mol⁺ subset, but did not induce suppression by the T8⁺Mol^- subset. In contrast, NK and LAK activity was exclusively found in the T8⁺Mol⁺ subset of cells but not in the T8⁺Mol^- subset of cells. These results suggest that the CD11 molecule is useful for distinguishing novel subsets of T8 cells. © 1988.

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Suppression of in vitro production of anti-U1-ribonucleoprotein antibody by monoclonal anti-idiotypic antibody to anti-U1-ribonucleoprotein antibody

Koide J., Takeuchi T., Hosono O., Takano M., Abe T.

Scandinavian Journal of Immunology 28 （ 6 ） 687 - 696 1988年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0300-9475

We produced monoclonal anti-idiotypic antibody against immunoaffinity purified anti-U1-ribonucleoprotein (RNP) antibody from a patient (K.T.), by the cell fusion procedure. The specificity of monoclonal anti-idiotypic antibody (IgG1, κ) was determined by inhibition studies. With the monoclonal anti-idiotypic antibody, cross-reactive idiotypes on anti-U1-RNP antibodies from unrelated patients with anti-U1-RNP antibody was detected in 57% of the samples. The anti-idiotypic antibody specifically suppressed the in vitro production of anti-U1-RNP antibody by lymphocytes from the patient K.T., and unrelated patients with a cross-reactive idiotype, in whom idiotype-reactive T cells were demonstrated. The results indicate that anti-idiotypic antibody may modulate the regulation of in vitro anti-U1-RNP antibody production.

Development of an antigen-specific CD8 suppressor effector clone in man

Takeuchi T., Schlossman S. F., Morimoto C.

Journal of Immunology 141 （ 9 ） 3010 - 3015 1988年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0022-1767

A long-term cultured IL-2-dependent keyhole limpet hemocyanin (KLH)-specific CD8 (T8) suppressor clone (5B9) was generated from a healthy donor hyperimmunized with KLH. The 5B9 clonal population suppressed in vitro anti-KLH antibody response but did not suppress anti-TT antibody response or PWM-driven IgG synthesis. Moreover, 5B9 cells could not suppress anti-TT antibody response even in the presence of free KLH. 5B9 cloned cells suppressed the anti-KLH antibody response of B cells cultured with CD4⁺4B4⁺ cells without requiring the presence of CD8⁺ cells. This KLH-specific CD8 suppressor clone is an effector type rather than an inducer type of suppressor T cell. The cloned cells expressed α- and β-TCR proteins (defined by WT-31 antibody) on their cell surface. More importantly, the CD3:TCR complex was functionally important in the suppression induced by this clone, because after CD3 antigen modulation from its cell surface, the suppressor effector function was abolished.

Defective expression of the 2H4 molecule after autologous mixed lymphocyte reaction activation in systemic lupus erythematosus patients

Takeuchi T., Tanaka S., Steinberg A. D., Matsuyama T., Daley J., Schlossman S. F., Morimoto C.

Journal of Clinical Investigation 82 （ 4 ） 1288 - 1294 1988年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0021-9738

Previous studies demonstrated that patients with active systemic lupus erythematosus (SLE), especially those with active renal disease, had a marked reduction in T4⁺2H4⁺ suppressor inducer cells in their peripheral blood. However, it was puzzling to find that active SLE patients without renal diseases often had normal percentages of T4⁺2H4⁺ cells. In the present study, we attempted to determine whether active SLE patients bearing normal percentages of T4⁺2H4⁺ cells had a defect in their expression of the 2H4 molecule on T4⁺ cells after autologous mixed lymphocyte reaction (AMLR) activation. The peripheral blood lymphocytes (PBL) from 50 SLE patients with normal percentages of T4⁺2H4⁺ cells (≥7% in PBL) were studied and the results were compared with those of 40 normal individuals. The density of the 2H4 molecule on T4 cells from normal controls increased during the 7-d AMLR; in contrast T4 cells from patients with SLE, especially those with active SLE, had defective expression of the 2H4 antigen after AMLR activation. Patients with inactive SLE, like normals, showed an increase in the 2H4 molecule after AMLR activation. Moreover, a strong correlation was observed between percent suppression of pokeweed mitogen (PWM)-driven IgG synthesis and the density of the 2H4 antigen on AMLR-activated T4 cells. Serial analysis of patients with SLE showed that the density of the 2H4 antigen expression and the suppressor inducer activity of AMLR-activated T4 cells were inversely correlated with disease activity. Thus, defective expression of the 2H4 antigen may be an important mechanism for the failure of active SLE patients with normal percentages of T4⁺2H4⁺ cells to generate suppression.

DEFECTS OF AUTOLOGOUS MIXED LYMPHOCYTE REACTION-ACTIVATED IMMUNOREGULATORY T-CELLS IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS

竹内勤

Scandinavian Journal of Immunology 26 （ 4 ） 363 - 369 1987年10月

研究論文（学術雑誌）, 査読有り, ISSN 0300-9475

THE T4 MOLECULE DIFFERENTIALLY REGULATING THE ACTIVATION OF SUBPOPULATIONS OF T4+ CELLS

竹内勤

Journal of Immunology 139 （ 3 ） 665 - 671 1987年08月

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0022-1767

THE 2H4 MOLECULE BUT NOT THE T3-RECEPTOR COMPLEX IS INVOLVED IN SUPPRESSOR INDUCER SIGNALS IN THE AMLR SYSTEM

竹内勤

Cellular Immunology 107 （ 1 ） 107 - 114 1987年06月

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0008-8749

A DEFECT OF IMMUNOREGULATORY T-CELL SUBSETS IN SYSTEMIC LUPUS-ERYTHEMATOSUS PATIENTS DEMONSTRATED WITH ANTI-2H4 ANTIBODY

竹内勤

Journal of Clinical Investigation 79 （ 3 ） 762 - 768 1987年03月

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0021-9738

INDUCTION OF SUPPRESSION FOLLOWING AUTOLOGOUS MIXED LYMPHOCYTE-REACTION - ROLE OF A NOVEL 2H4 ANTIGEN

竹内勤

European Journal of Immunology 17 （ 1 ） 97 - 103 1987年01月

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0014-2980

The 2H4 molecule but not the T3-receptor complex is involved in suppressor inducer signals in the AMLR system

Takeuchi Tsutomu, Schlossman Stuart F., Morimoto Chikao

Cellular Immunology 107 （ 1 ） 107 - 114 1987年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0008-8749

It is suggested that autologous mixed lymphocyte reaction (AMLR) may play an important role in generating suppressor inducer signals and in down-regulating the immune response following self-major histocompatibility recognition. In the present study, monoclonal antibodies directed at cell surface structures on T4+ cells activated in AMLR were used to define the molecules important in the generation of the suppressor inducer signal. The density of a 200 220-kDa structure, termed 2H4, increased on T4 cells during activation in AMLR and furthermore a strong correlation was observed between the generated suppressor inducer activity of such cells and the density of the 2H4 antigen. More importantly, we showed that treatment of AMLR activated T4 cells with anti-2H4 but not anti-T3 or T4 antibody abolished the suppressor inducer function of these cells. These results suggest that the 2H4 molecule but not the T3-receptor complex plays an important role in generating suppressor inducer signals in the AMLR system. © 1987.

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A defect of immunoregulatory T cell subsets in systemic lupus erythematosus patients demonstrated with anti-2H4 antibody

Morimoto C., Steinberg A. D., Letvin N. L., Hagan M., Takeuchi T., Daley J., Levine H., Schlossman S. F.

Journal of Clinical Investigation 79 （ 3 ） 762 - 768 1987年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0021-9738

The cell surface phenotype of peripheral blood lymphocytes (PBL) of systemic lupus erythematosus (SLE) patients was characterized with the anti-2H4 monoclonal antibody that defines the human suppressor inducer subset. The T4⁺2H4⁺ population of cells has been shown to be critical for the activation of T8⁺ suppressor cells. Patients with SLE had a markedly decreased percentage of T4⁺2H4⁺ cells (13 ± 2%) in their PBL compared with normal controls (21 ± 1%) (P < 0.001). This reduction was greatest in patients with active SLE, especially those with renal disease. Serial analysis of patients with SLE and renal disease showed a correlation between percent positive circulating T4⁺2H4⁺ cells and disease activity. Moreover, there was a significant correlation between a low percentage of T4⁺2H4⁺ cells and decreased suppressor-inducer function in autologous mixed lymphocyte reaction-activated T4⁺ cells from SLE patients. Thus, a deficiency exists in SLE patients with active renal disease in the T4⁺2H4⁺ suppressor-inducer T cell subset.

Defects of autologous mixed lymphocyte reaction-activated immunoregulatory T cells in patients with systemic lupus erythematosus

Koide J., Takeuchi T., Hosono O., Takano M., Abe T.

Scandinavian Journal of Immunology 26 （ 4 ） 363 - 369 1987年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0300-9475

The present study was undertaken to determine the nature of the immunoregulatory T-cell defect after autologous mixed lymphocyte reaction (AMLR) activation in patients with systemic lupus erythematosus (SLE). Although AMLR was decreased in patients with SLE compared with normals, there was no difference in major proliferative cells (T4 cells and T4⁺JRA⁺ subset) in response to AMLR. Functional activity of AMLR-stimulated T4 subsets in patients with SLE and normals was examined in helper and suppressor/inducer assay, using pokeweed mitogen (PWM)-derived IgG synthesis. The T4⁺JRA^- (helper) subset from SLE patients showed no greater activity than normals. However, the T4⁺JRA^- (helper) subset from SLE patients showed no greater activity than normals. However the T4⁺JRA⁺ (suppressor/inducer) subset from SLE patients showed decreased suppression induction compared with normals. This defect in the suppressor/inducer function was demonstrated even in patients with inactive SLR or in remission.

The T4 molecule differentially regulating the activation of subpopulations of T4⁺ cells

Takeuchi T., Schlossman S. F., Morimoto C.

Journal of Immunology 139 （ 3 ） 665 - 671 1987年

研究論文（学術雑誌）, 共著, 査読有り, ISSN 0022-1767

It has been demonstrated that the T4⁺2H4⁺ subset functioned as a suppressor inducer cell, whereas the reciprocal T4⁺2H4^- subset provided help for B cell Ig production. In the present studies, a series of monoclonal antibodies to cell surface structures expressed on subsets of cells were examined for their effects on the proliferative and immunoregulatory functions generated in AMLR. We demonstrated that anti-T4 antibody preferentialy inhibited the proliferative response of the T4⁺2H4⁺ but not T4⁺2H4^- cells against self-MHC antigens. In contrast, anti-T3 and anti-Ia antibodies inhibited the response of both subsets of cells. This subset preference of anti-T4 antibody was not attributable to either the isolation procedures used or a shift in the kinetics of proliferation to autologous self-MHC antigens. Moreover, both IL 2 production and the immunoregulatory function of the T4⁺2H4⁺ subset was profoundly inhibited by anti-T4 antibody, whereas the T4⁺2H4^- subset was minimally influenced. In the absence of Ia molecules, T4⁺2H4⁺ but not T4⁺2H4^- cell proliferation was inhibited with anti-T4 antibody. Together, these results suggest that the T4 molecule plays a distinct functional role in the differential triggering of subsets of T4⁺ cells.

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