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Biomedical subjects

J Yata

Publications and source records attributed to J Yata.

At least 145 records · Page 8Linked to original sources
PubMed1982

In vitro detection of anti-thyroglobulin antibody forming cells from the lymphocytes of chronic thyroiditis patients and analysis of their regulation.

Anti-thyroglobulin (anti-Tg) antibody forming cells were detected by plaque forming cell (PFC) assay, using B cells depleted of sheep erythrocyte (SRBC) binding cells and T cells separated without SRBC interaction. When 2 x 10(5) non-T cells were combined with the same number of T cells from chronic thyroiditis patients, more than 20 PFC were detected; few, if any, PFC developed from normal lymphocytes. T cells were generally needed to produce quantifiable PFC, suggesting that helper T cells are required for this autoantibody formation. A positive relationship existed between the number of PFC and the serum anti-Tg antibody titres of the same patients. The generation of Tg-specific PFC from patient lymphocytes was markedly suppressed by normal T cells or T cells from patients whose lymphocytes did not produce PFC. The same level of suppression was also seen on the addition of culture supernatant from Tg antigen stimulated T cells. Autologous T cells, from patients whose lymphocytes produced PFC, did not show such suppressor effects, suggesting that in chronic thyroiditis patients, the regulatory T cell function preventing anti-Tg autoantibody formation is impaired.

Antibodies, Anti-Idiotypic↗
PubMed1981

Primary immunodeficiency syndrome in Japan. I. Overview of a nationwide survey on primary immunodeficiency syndrome.

The results of a nationwide survey on primary immunodeficiency syndrome (PIS) in Japan are presented. By the repeated questionnaire method, 497 PIS cases were collected prior to February 1979 with clinical information. Numbers of each type of PIS, age at the time of diagnosis, patient's status at the time of registration, familial incidence of PIS, and development of malignancy, autoimmune diseases, and allergic diseases among all reported patients are presented and discussed.

Adolescent↗
PubMed1981

Immune complex-dependent T cell-mediated cytostasis (IDTC).

The growth of human lymphoid cell lines was suppressed by human peripheral T cells in the presence of immune complexes (IC). T cells bearing IgG receptors (TG cells) were, but T-non-G cells and non-T cells were not, active as effectors of cytostasis which was induced by IC-mediated bridging of the target and effector cells via Fc receptors. We propose that this phenomenon be called 'immune complex-dependent T cell-mediated cytostasis' (IDTC) and suggest its possible role in IC-mediated tissue injury, especially where T cell infiltration is observed. TG cells from healthy individuals suppressed Ig production and were cytotoxic effectors upon interaction with IC. However, the cytotoxic effectors seem to be distinct from the suppressors of Ig production since TG cells from rheumatoid arthritis patients showed dissociation between these two functions: they displayed cytostasis but had only little suppressive effect on the B cell response.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1981

B and T cell involvement in anti-acetylcholine receptor antibody formation in myasthenia gravis.

The in vitro method of antibody production was applied to ascertain the contribution of B and T cells to the formation of anti-acetylcholine receptor (AChR) antibody. The anti-AChR antibody in the culture supernatant was estimated by radioimmunoassay, and the anti-AChR antibody-forming cells from cultures were detected by autoradiography of the antigen-binding cells. Thymic B cells from myasthenia gravis (MG) patients formed antibody when they were cultured with thymic T cells from MG patients and stimulated with AChR antigen. The antibody formation was more vigorous with thymic B cells, which contained more germinal centres. The antibody was also formed from the B and T cell combination of peripheral blood lymphocytes, although the amount was less than that produced by thymic lymphocytes from MG patients. The antibody produced by lymphocytes from MG patients. The antibody produced by lymphocytes from MG patients was suppressed by the addition of T cells from the culture supernatant of normal individuals, but not by autologous or allogeneic T cells from MG patients. The suppression by T cells from normal individuals was abolished when the cells were treated with mitomycin C. These observations indicated that AChR-specific B cells and helper T cells are active, while the suppressor T cells, which are usually present in normal individuals, are defective in MG patients.

Adult↗
PubMed1980

Age and seasonal variations in the serum levels of 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D in normal humans.

Serum concentrations of 25-hydroxyvitamin D (25-OH-D) and 24,25-dihydroxy-vitamin D [24,25-(OH)2-D] were measured in lipid extracts of 1 ml of human sera by a competitive protein binding assay. 25-OH-D and 24,25-(OH)2-D were isolated from th lipid extracts by Sephadex LH-20 column chromatography. The 24,25-(OH)2-D fraction on the Sephadex LH-20 columns were further purified by high pressure liquid chromatography prior to assay. Serum levels of 25-OH-D and 24,25-(OH)2-D in normal males were similar to those in normal females throughout each age group. Serum levels of 25-OH-D and 24,25 (OH)2-D in newborns were 8.28 +/- 1.68 ng/ml (mean +/- SD) and 0.55 +/- 0.16 ng/ml, respectively, which were significantly (p<0.001) lower than those in adults (21.3 +/- 4.8 ng/ml of 25-OH-D and 1.55 +/- 0.31 ng/ml of 24,25-(OH)2-D). A seasonal variation was demonstrated in serum levels of 24,25-(OH)2-D as well as those of 25-OH-D. Serum levels of 24,25-(OH)2-D were highly correlated (gamma=0.884, p<0.001) with those of 25-OH-D in normal human subjects, and the percentage ratio of 24,25-(OH)2-D/25-OH-D was 7.4 +/- 1.4% (mean +/- SD), irrespective of age or seasonal variations.

24,25-Dihydroxyvitamin D 3↗