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Biomedical subjects

O Hosono

Publications and source records attributed to O Hosono.

At least 37 records · Page 2Linked to original sources
PubMed1989

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

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 micrograms of CCA per milliliter suppressed PHA- and AMLR-stimulated 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.

Adjuvants, Immunologic↗
PubMed1988

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

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 synthesis. Increased anti-nRNP antibody synthesis may be due to increased T4-helper cell function rather than defective T8-suppressor function.

Adult↗
PubMed1988

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

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, kappa) 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.

Animals↗
PubMed1987

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

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)-driven IgG synthesis. 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.

Adult↗
PubMed1986

DNA-daunorubicin complexes specifically suppress in vitro spontaneous anti-DNA antibody production in lymphocytes of patients with systemic lupus erythematosus.

Elevated production of anti-DNA antibody in patients with systemic lupus erythematosus (SLE) is a central problem in the pathogenesis of tissue injury. In the present study, we attempted to manipulate anti-DNA antibody production through the antigen-cytotoxic drug conjugates, DNA-daunorubicin complexes. The effect of DNA-daunorubicin complexes was determined by examining SLE lymphocytes for spontaneous in vitro production of anti-DNA antibody. These complexes, at 2 micrograms/ml, suppressed anti-DNA antibody production, but not total IgG production, which suggests that specific suppression of anti-DNA antibody production was achieved at this concentration. We believe that the DNA-daunorubicin complexes affected mainly B cells, since such suppression was obtained by treating B cells, as well as B plus T cells. Furthermore, the complexes had no effect on the proliferative responses of SLE T cells to DNA, phytohemagglutinin, or concanavalin A. These results indicate that DNA-daunorubicin complexes may have the potential for selectively suppressing anti-DNA antibody production in patients with SLE.

Antibodies, Antinuclear↗
PubMed1986

Direct demonstration of immunoregulatory T-cell defects in patients with systemic lupus erythematosus.

The present study was undertaken to determine directly whether immunoregulatory T cells have a defective suppressor function in patients with systemic lupus erythematosus (SLE), and whether anti-T-cell antibodies are essential for immunoregulatory T-cell defects. Peripheral blood T cells and T-cell subsets were determined in 52 SLE patients. The ratio of T4 to T8 cells was distributed over a wider range in patients with SLE than in the controls. Patients with SLE were divided into three groups (low, normal and high) by the T4/T8 ratio. Lymphocytes from 12 SLE patients (7 with low and 5 with high T4/T8 ratios) were studied extensively. Their disease was inactive or in remission. Anti-T-cell antibodies were not detected, and yet the patients had immunological abnormalities characterized by the presence of antinuclear antibodies and hypergammaglobulinaemia. The SLE patients with high T4/T8 ratios had a decreased number of T8 cells, and defective suppressor-effector cells. In contrast, patients with low T4/T8 ratios had decreased T4 cells and/or increased T8 cells, and defective suppressor-inducer cells. Two patients with low T4/T8 ratios had both suppressor-effector and suppressor-inducer cell defects. These results indicate that immunoregulatory circuits in SLE patients are heterogeneous and that immunoregulatory defects exist even when the disease is inactive or in remission. Anti-T-cell antibodies were not essential for such immunoregulatory defects. Thus, immunoregulatory T-cell defects and the development of SLE may be independent conditions due to other unknown causes.

Adult↗
PubMed1985

[Comparative studies on immunological property of thyroglobulins obtained from the thyroid tumor and the adjacent tissue].

The immunological properties of thyroglobulins (Tg) of individual patients, obtained from a thyroid tumor and its adjacent tissue were compared, using conventional or monoclonal antibodies against human Tg. The thyroid tumors studied were non-functioning thyroid carcinomas and functioning thyroid adenomas. In contrast to non-functioning tumors, Tg from the functioning tumors was generally iodinated at a level close to that of normal tissue, and Tg from the tissue adjacent to the tumors had a very low iodine content. The conventional antiserum and monoclonal antibodies, B2F, seemed to recognize the conformation of Tg, while C6G showed a high affinity to Tg even when unfolded or denatured. In most cases, Tg isolated from the tissue adjacent to a tumor showed a higher affinity to antibodies than Tgs of the tumor tissue, as determined by the inhibitional effect of these Tgs against the binding of standard Tg and antibody. Furthermore, the Tg of the adjacent tissue was immunologically different in nature from the standard Tg obtained from a normal thyroid gland. From these results, Tgs of tumor and the adjacent tissue in individual patients were heterogeneous in immunological property, regardless of iodine content.

Adenocarcinoma↗
PubMed1985

[The immunochemical properties of thyroglobulin in human thyroid tumors in reaction to rabbit anti-human normal thyroglobulin-serum].

Interactions between antiserum (rabbit anti-human normal thyroglobulin-serum) and human thyroglobulin preparations (obtained from the tissues of the normal thyroid gland, thyroid adenoma, and carcinoma) were compared by inhibition effect with the binding between 131I-labeled standard thyroglobulin and antiserum, set up by a double antibody RIA. Thyroglobulins isolated from normal glands (designated as Nor-Tg) have a high affinity to the antiserum. In contrast, thyroglobulins in follicular adenoma or adenomatous goiter (designated as Ad-Tg) decrease the potency of the affinity to the antiserum. Furthermore, thyroglobulins in papillary or follicular carcinoma (designated as Ca-Tg) markedly decrease such a potency. With the t-test, the inhibition curves of Nor-Tgs are almost parallel to each other. Most of the inhibition curves of Ad-Tgs and Ca-Tgs are not parallel to the curve of Nor-Tg 1 (P-value for non-parallelism less than or equal to 0.05). Therefore, it seems that Tg preparations obtained from tumor tissue are heterogeneous in terms of specificity and/or affinity to antiserum, judging from the results of the non-parallel inhibition curves. The present results also show that the contribution of iodine content in Tg has little or no effect on the nature of Tg-immunogenicity.

Adenoma↗
PubMed1985

Suppression of rheumatoid factor synthesis by antiidiotypic antibody in rheumatoid arthritis patients with cross-reactive idiotypes.

The effect of antiidiotypic antibody on the in vitro production of rheumatoid factor was studied in rheumatoid arthritis patients with cross-reactive idiotypic determinants. Antiidiotypic antibodies (ascites IgG) were developed against monoclonal rheumatoid factor (Ka m-RF) by a cell fusion procedure. These antibodies were idiotype-specific, since: 1) they reacted only with F(ab')2 fragment of Ka m-RF; 2) they failed to react with normal IgM without rheumatoid factor activity; and 3) their F(ab')2 fragment inhibited the rheumatoid factor activity of Ka m-RF. The antiidiotypic antibody strongly suppressed the in vitro production of rheumatoid factor by lymphocytes from unrelated rheumatoid arthritis patients with cross-reactive idiotypes. The suppression was specific, since ascites IgG failed to suppress in vitro anti-keyhole limpet hemocyanin antibody production by the lymphocytes. These results indicate that antiidiotypic antibody may influence the regulation of rheumatoid factor production in patients with rheumatoid arthritis.

Antibodies, Monoclonal↗
PubMed1984

Suppressor T cell function in patients with rheumatoid arthritis complicated by vasculitis.

Concanavalin A (Con A)-induced suppressor T cell activity was determined in 10 rheumatoid arthritis (RA) patients with vasculitis, 34 RA patients without vasculitis, and 10 healthy individuals. The percent Con A-induced suppression in RA patients with vasculitis was 24.6. In contrast, it was 68.4% in those RA patients without vascular lesions. Further, the proportion of T cells reactive with OKT8 monoclonal antibody was also decreased in RA patients with vasculitis. Accordingly, the reduced Con A-induced suppressor T cell activity in these RA patients resulted, in part, from the reduction in the number of cells of the suppressor T cell subset. Those patients with vascular lesions also had a higher percentage of positive antilymphocytotoxic antibodies than RA patients without vasculitis. Since the differences in Con A-induced suppressor T cell activity and frequency of positive antilymphocytotoxic antibodies were so great, we believe RA patients with vasculitis could be recognized as a disease group distinct from RA patients without vasculitis.

Adult↗
PubMed1984

Cellular mechanism of DNA-specific antibody synthesis by lymphocytes from systemic lupus erythematosus patients.

The cellular mechanism of anti-DNA antibody synthesis in patients with systemic lupus erythematosus (SLE) was studied by DNA-specific solid-phase radioimmunoassay. Anti-DNA antibody synthesis in response to DNA was T-dependent, and the experiments with reconstituted lymphocytes from identical twins discordant for SLE showed that B cells and T cells from SLE patients must cooperate to synthesize anti-DNA antibody. Anti-DNA antibody synthesis by lymphocytes from patients with inactive SLE was enhanced by T4 cells and suppressed by T8 cells in response to DNA. Although T4 cells from patients with active SLE could enhance anti-DNA antibody synthesis by autologous B cells, their T8 cells could not suppress anti-DNA antibody synthesis by autologous B cells. These results indicate that elevated anti-DNA antibody synthesis in response to DNA in patients with active SLE is due to abnormalities of both SLE B cells and SLE T cells. They further indicate that dysfunction of T8 cells from patients with active SLE may, in part, be responsible for deficient regulation of anti-DNA antibody synthesis.

Antibodies↗
PubMed1984

Anti-idiotypic antibodies in a patient with monoclonal rheumatoid factor after pneumococcal bacteremia.

A 51-yr-old Japanese female patient with monoclonal IgM gammopathy with rheumatoid factor activity was admitted because of pneumococcal bacteremia. About 2 wk after admission, her rheumatoid factor activity became undetectable by RAHA test and radioimmunoassay, subsequent to the initial marked elevation. The suppressive capacity of the patient's IgG fraction on the rheumatoid activity of her monoclonal IgM on January 11 was determined. The IgG fraction obtained on February 22 blocked the binding of the rheumatoid factor to rabbit IgG. The suppressive activity in the IgG fraction of February 22 was shown to be localized within the F(ab')2 fragment. Furthermore, the specificity of the suppressive serum factor was shown by the inability to block the binding of SRBC coupled with diazotized phosphorylcholine to anti-pneumococcal antibody. Thus, the marked reduction of rheumatoid factor activity was considered to result from anti-idiotypic antibody transiently appearing in her serum after pneumococcal bacteremia.

Antibodies, Anti-Idiotypic↗