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Biomedical subjects

T Tada

Publications and source records attributed to T Tada.

At least 307 records · Page 17Linked to original sources
PubMed1988

Metabolic disposition of ethyl eicosapentaenoate and its metabolites in rats and dogs.

When orally administered to rats, 14C-labelled ethyl eicosapentaenoate (14C-EPA-E) was hydrolyzed and, in the lymph, incorporated mainly into triglycerides (TG) in chylomicrons. In plasma and other tissues, eicosapentaenoic acid (EPA) and its metabolites, such as docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA), were detected in TG and phospholipid fractions. In plasma, EPA and its metabolites were found to be integrated into lipoproteins. Tissue distribution of these metabolites showed characteristic patterns from one tissue to another, as did their compositional distribution in lipids. EPA, DPA and DHA were found to be metabolized via beta-oxidation in in vitro experiments with mitochondrial fraction.

Acyl Coenzyme A↗
PubMed1988

I-J as a second T cell receptor for self--molecular polymorphism and the role in suppressive signal transduction.

We have been able to demonstrate an I-J epitope on the cell surface of interleukin 2 (IL-2) dependent T cell clones of both T helper (Th) and suppressor T cells (Ts) lineages by flow microfluorometry with fluoresceinated anti-I-Jk, and to identify the molecule by the specific immunoprecipitation and the gel analysis. The I-J molecule thus detected is a novel 90K dimeric molecule composed of 45K glycopeptide subunits distinct from conventional T cell receptor (TcR) or CD28. The molecule is not comodulated with TcR or T3 on the cell surface. Monoclonal anti-I-J can inhibit various major histocompatibility complex (MHC)-restricted T cell functions including Ca2+ influx, antigen-induced T cell proliferation and IL-2 production, indicating that the ligation of I-J molecules results in a negative signal transduction. Since it has been reported that the I-J phenotype undergoes a systematic adaptive alteration in radiation bone marrow chimeras in association with the acquired class II restriction, it is likely that I-J is a novel receptor for self MHC apart from TcR heterodimer and is required for a negative signal transduction.

Animals↗
PubMed1988

[Hyperfunctioning follicular carcinoma of the thyroid. A case report].

A 76-year-old female patient with a large neck lump of 15-year duration, was accompanied by palpitation and tremor. The lump was 9 x 5cm in size and the lower half of it was not palpable because the lower pole was located in the mediastinum. Physical examination revealed two enlarged lymph nodes in the right supraclavicular area. Chest X-ray film showed a coin lesion in the right lung that seemed to be a metastasis. The patient was apparently thyrotoxic with elevated serum concentrations of 15.7 micrograms/dl thyroxin and 359 ng/dl triiodothyronine. A neck scintigraphy using 123Iodine showed a thyroid hot nodule in accordance with this lesion. A total thyroidectomy with a modified neck dissection was carried out. This was followed by 131Iodine therapy. Specimen of the primary lesion weighed 147 g. Pathology of this tumor was follicular carcinoma of the thyroid. The patient was doing well 14 months after surgery. In the literature, three cases of similar hyperfunctioning thyroid carcinoma have been reported, all of which had a large primary lesion. The histological features proved to be of follicular or papillofollicular type. The treatment in these cases was administration of an antithyroid drug followed by surgical removal.

Adenocarcinoma↗
PubMed1987

Major histocompatibility complex-restricted augmenting T cells induced by in vitro cultivation of antigen-primed T cells. A new parallelism between suppressor and augmenting circuits.

In vitro cultivation of primed T cells with antigen resulted in the induction of a regulatory T cell that nonspecifically augmented the in vitro antibody responses of H-2-compatible T and B cells. This T cell, designated as the augmenting T cell (Ta), was unable to help B cells by itself but enhanced the antibody response of B cells to several multitudes only when conventional helper T (Th) cells or cloned Th cells from the same H-2 haplotype coexisted. Ta was radioresistant and belonged to Lyt-1+, 2-, L3T4+, I-J- T cell lineage. Ta exhibited interesting H-2-restricted activities: when primed T cells from (A X B) F1 were cultured with the antigen in the presence of parent A type antigen-presenting cells, the induced Ta was able to augment the antibody response of (A x B) F1 B cells in the presence of Th cells from F1----A but not from F1----B radiation bone marrow chimeras. This indicates that the induction of Ta in an F1 T cell population is dependent on the H-2 haplotype of antigen-presenting cells during in vitro cultivation. The restriction specificity of the established Ta is, however, not directed to the class II antigen itself but to the restriction specificity of Th cells that recognize class II antigen. In support of this is the fact that the elimination of A-restricted Th cells during cultivation by treatment with anti-I-J mAb, which is known to react with H-2-restricted Th cells, resulted in failure of induction of Ta cells having the augmenting activity for the A-restricted response.

Animals↗
PubMed1987

Epitopes associated with MHC restriction site of T cells. III. I-J epitope on MHC-restricted T helper cells.

I-J epitopes were found to be associated with the functional site of the class II MHC-restricted helper T (Th) cells: Virtually all of the H-2k-restricted Th cell function of H-2kxbF1 T cells was inhibited by the anti-I-Jk mAb, leaving the H-2b-restricted function unaffected. The I-Jk epitope was inducible in Th cells of different genotype origin according to the environmental class II antigens present in the early ontogeny of T cells. Although above results suggested that I-J is the structure reflecting the inducible MHC restriction specificity, further studies revealed some interesting controversies: First, the I-J phenotype did not always correlate with the class II restriction specificity, e.g., I-Ab-restricted Th from 5R was I-Jk-positive, whereas I-Ak-restricted Th of 4R was not. Second, there was no trans expression of parental I-J phenotypes and restriction specificities in F1 Th, e.g., the I-J phenotype was detected only on I-Ab-restricted Th of (4R X 5R)F1, whereas it was absent on I-Ak-restricted Th. This strict linkage between the restriction specificity and I-J phenotype was also found on Th cells developed in bone marrow chimera constructed with intra-H-2-recombinant mice. The expression of I-Jk was always associated with the restriction specificity of the relevant host. Thus, the restriction specificity of Th cells followed the host type, and the I-J expression on Th was exactly the same as that expressed by the host haplotype. These results indicate that I-J is an isomorphic structure adaptively expressed on Th cells that is involved in the unidirectional regulatory cell interactions, and that the polymorphism cannot be explained merely by the restriction specificity of the conventional T cell receptor heterodimer.

Animals↗
PubMed1987

MHC-restricted minimal regulatory circuit initiated by a class II-autoreactive T cell clone.

The in vivo administration of a self-class II-reactive Th clone MS202 derived from C3H into syngeneic mice resulted in the suppression of both primary and early secondary antibody responses against T cell-dependent antigens. The suppression was due to the generation of antigen-nonspecific Ts cells in the recipient, as the splenic T cells from the mice treated with MS202 were able to strongly suppress the in vitro secondary antibody response of primed syngeneic spleen cells. The dose-response curve of suppression indicated the generation of an effector type Ts that directly suppressed Th. The surface phenotype of Ts was Ly-1+,2-, L3T4+, I-J-. The presence of Ly-1+,2+ T cells was not required to induce the suppression. The suppression was strictly restricted to H-2k, as F1 Ts cells were able to suppress the response of C3H but not of B6 B cells helped by the same F1 Th cells. The experiments with chimeric mice indicated that the direct target of Ts is an MHC-restricted Th but not a B cell or APC. The results indicate the existence of a minimal regulatory circuit where an MHC-restricted Th induces a preprogrammed Ts that in turn directly suppresses Th with the same MHC-restriction specificity. The induction of and suppression by Ts appeared to be due to the direct recognition of MHC restriction sites of Th cells.

Animals↗
PubMed1987

Epitopes associated with the MHC restriction site of T cells. I. Selective expression of Iat epitopes on H-2-restricted helper T cells.

We previously established monoclonal antibodies (mAb) that are putatively directed to the I region of H-2k but are reactive only with T cells. Because of their specificity to the unique epitopes different from class II antigens, they are designated as anti-Iat reagents. The present study demonstrated that these anti-Iat inhibit the H-2k-restricted helper T (Th) cell function by acting on the very H-2 restriction site of both H-2k and H-2kxb F1 T cells. This was determined by both the cytotoxic treatment and blocking of antigen-primed Th cells. In the F1 Th population, only those restricted to H-2k were eliminated, leaving the H-2b-restricted Th cells uninhibited. The inhibition of the response was not due to the induction of suppressor T cells, but to the elimination of the function of radioresistant Lyt-1+,2- Th cells. Iatk epitopes were also found on an H-2k-restricted but not on H-2b-restricted Th cell clone established from the same H-2kxb F1 animal. None of the anti-Iatk were reactive with class II antigens on B cells. These results indicate that Iat epitopes are not directly encoded by the I region genes, but are associated with the H-2 restriction site of T cells, which see the self class II polymorphism. Thus, Iat epitopes are expressed clonally in high frequency on H-2k-restricted Th cells of F1, being excluded from the H-2b-restricted Th population. The relationship between Iat and T cell receptor molecules is unknown.

Animals↗
PubMed1987

Analysis of two distinct B cell activation pathways mediated by a monoclonal T helper cell. I. MHC-restricted activation of B cells by an IL 2-dependent pathway.

The present study was carried out to determine whether the MHC-restricted and MHC-unrestricted B cell activation pathways mediated by a single cloned Th cell are separable, and whether these two pathways are mediated by distinct mechanisms. It was demonstrated that the two B cell activating functions of a single cloned Th cell could be separated by their sensitivity to irradiation. It was shown that MHC-restricted B cell activation is mediated by a radiosensitive Th cell function, whereas MHC-unrestricted B cell activation is mediated by a radioresistant function of the same Th cell. In addition, it was shown that recombinant IL 2 can restore or replace the radiosensitive component of MHC-restricted cognate helper function.

Animals↗
PubMed1987

Epitopes associated with the MHC restriction site of T cells. II. Somatic generation of Iat epitopes on T cells in radiation bone marrow chimeras.

We described in this paper systematic alterations in the expression of unique I region controlled epitopes on helper T cells (Th) in chimeras according to the changes in their H-2 restriction specificity. Taking advantage of the reactivity of monoclonal antibodies (anti-Iat) putatively specific for the epitopes indirectly controlled by I region and expressed in association with the Iak restriction site of Th, we examined the alterations of these epitopes on Th cells from various bone marrow chimeras. Iatk epitopes were physiologically expressed on Iak-restricted but not on Iab-restricted Th cells in (H-2k X H-2b)F1 mice. In the chimeric condition, the H-2k-restricted Th of B6----F1 chimera acquired the expression of Iatk even though B6 Th is unable to express Iatk when developed under the physiologic condition. Iatk are also found on Th of fully allogeneic chimera of B6----C3H, whereas Th cells of C3H----B6 completely lost the Iatk expression. These results indicate that Iat epitopes originally defined as unique I region-controlled determinants selectively expressed on T cells are not encoded by the I region genes but are associated with the T cell receptor that sees the self Ia. The epitopes undergo the adaptive alterations according to the acquisition of a new MHC restriction. This is the first example to demonstrate the epitope associated with T cell receptor which undergo the systematic adaptive differentiation.

Adaptation, Physiological↗
PubMed1987

Shared idiotopes between anti-class II monoclonal antibodies and major histocompatibility complex recognition site of T cells.

We have raised a number of monoclonal antibodies (mAb) against idiotopes (Id) on monoclonal anti-murine class II (anti-Ak or Ek) antibodies. Two anti-Id mAb among 31 were found to cross-react with some T cells but not with macrophages and B cells of H-2k animals. They were able to block syngeneic mixed lymphocyte reaction (SMLR) and antigen-induced major histocompatibility complex (MHC)-restricted T cell proliferation of H-2k but not of other haplotypes. These results indicated that antibodies were recognizing Id associated with the MHC restriction site of T cells. The injection of these anti-Id mAb into H-2k mice resulted in the stimulation of self-class II-reactive T cell clones as determined by SMLR. They were also able to stimulate in non-H-2k strains to prime H-2k alloreactive T cell clones. Some animals developed anti-class II (anti-Iak) antibodies by the injection of anti-Id. These results indicated that certain anti-Id (anti-anti-class II) antibodies cross-reacted with T cell receptors which carried class II restriction specificity and were involved in allorecognition. These antibodies were found to have an ability to alter the T cell repertoire in vivo by stimulating such MHC-restricted clones.

Animals↗
PubMed1987

A comparative study of alteration in lymphocyte subsets among varicella, hand-foot-and-mouth disease, scarlet fever, measles, and Kawasaki disease.

Changes in the lymphocyte subsets of 13 patients with varicella, 5 with hand-foot-and-mouth disease, 4 with scarlet fever, 10 with measles and 20 with Kawasaki disease were examined by immunofluorescent flow cytometric analysis using monoclonal antibodies against lymphocyte cell surface antigens. The results were compared with those of age-matched normal controls. A significant increase in the percentage of Leu-2a positive (Leu-2a+) cells was shown during the early convalescence of varicella, scarlet fever and measles. A significant decrease in the percentage of Leu-3a+ cells during the acute phase was common to all the diseases examined, and a significant decrease of Leu-4+ cells was observed except in measles. As a result, a significant decrease in the Leu-3a+/Leu-2a+ ratio was common to all the diseases examined during the acute and/or early convalescent phases. Leu-M3+ cells increased significantly in varicella, scarlet fever, and Kawasaki disease. HLA-DR+ cells increased significantly in varicella and Kawasaki disease. No significant changes in the proportions of Leu-7+, Leu-10+, and 2H7+ cells were found throughout the course of all the diseases examined.

Adolescent↗