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T Tada

Publications and source records attributed to T Tada.

At least 379 records · Page 21Linked to original sources

Idiotypic and fine specificity analysis of a (4-hydroxy-3-nitrophenyl)acetyl (NP)-specific suppressor T cell hybridoma at the level of cell surface structures, isolated receptor material and functional suppressor factor.

The (4-hydroxy-3-nitrophenyl)acetyl (NP)-specific T suppressor cell hybridoma 7C3-13 was established by fusing splenic B10.BR T cells enriched on NP-coated petri dishes with the AKR thymoma BW5147. 7C3-13 was selected by anti-NPb idiotypic and anti-I-Jk antibodies in microcytotoxicity tests. The hybridoma expressed H-2k, I-Jk, Qa-1, Thy-1.1 as well as idiotypic (binding site-related) and framework Ig VH determinants, while it was negative for I-A, I-E/C, Thy-1.2, Lyt-1, Lyt-2 and Ig constant region determinants. Hapten-binding receptor material could be isolated from 7C3-13 cells on NP-coupled nylon nets and functionally active T suppressor factor (TsF) could be extracted from the hybridoma. Both types of soluble molecules express NPb idiotype, but the TsF carries I-J determinants in addition while the isolated receptors do not. The molecular weight of the isolated receptor material is 80 000, that of the TsF activity is 27 000 and 57 000-64 000, respectively. We thus were able to show that NP-binding molecules can be obtained in the form of cellular surface receptors, isolated receptor material and extracted TsF from one and the same, monoclonal, cell source.

Animals↗

RNA transcripts for I-J polypeptides are apparently not encoded between the I-A and I-E subregions of the murine major histocompatibility complex.

The I-J subregion of the mouse major histocompatibility complex has been reported to encode antigenic determinants expressed by suppressor T cells. Previously, cosmid clones were obtained from mouse sperm DNA that contain all of the sequences between the I-A and I-E subregions, where I-J has been mapped genetically. However, hybridization of these sequences to RNA prepared from several I-J-positive suppressor T-cell hybridomas did not reveal the presence of a transcript. In addition, no rearrangements in this DNA were detected in the suppressor T cells that we have analyzed. Our results indicate that the I-J polypeptides are not encoded between the I-A and I-E subregions of the major histocompatibility complex. We discuss several hypotheses concerning the possible location and expression of I-J genes.

Animals↗

Structural analysis of antigen-specific Ia-bearing regulatory T-cell factors: gel electrophoretic analysis of the antigen-specific augmenting T -cell factor.

An antigen-specific T-cell factor (TaF) that specifically augments the antibody response was purified and biochemically analyzed by NaDodSO4/polyacrylamide gel electrophoresis and isoelectric focusing. Biosynthetically labeled TaF was separated from the Nonidet P-40 extract of T-cell hybridoma FL10, which produces a keyhole limpet hemocyanin-specific TaF, by affinity chromatography either with antigen or with monoclonal anti-I-A antibodies. The material thus obtained was composed of two different types of molecules of molecular weights of 67,000 and 33,000 under nonreducing conditions. After reduction with dithiothreitol, all the molecules migrated to the position of molecular weight 33,000. The absorption studies with immunoadsorbents of antigen and antibodies revealed that the intact TaF is a heterodimer of two discrete polypeptide chains, one carrying a determinant detectable by a monoclonal anti-Tindd directed to an Igh-I -linked allotypic structure of T cells and being associated with the antigen-binding site and the other expressing a unique determinant controlled by the I-A subregion of murine H-2 major histocompatibility complex but being different from known class II polypeptide chains. The antigen-binding polypeptide has an isoelectric point of pH 5.6, and the I-A polypeptide has an isoelectric point of pH 6.3.

Aged↗

Evidence for two suppressor factors secreted by a single cell suggests a solution to the J-locus paradox.

The hybridoma produced by the fusion of lactate dehydrogenase-B (LDH-B)-primed B10.A(2R) mouse suppressor T (Ts) cells with the BW5147 thymoma secretes two kinds of T suppressor factors (TsF), TsF-A and TsF-E. The TsF-A suppresses A beta-restricted and the TsF-E, E beta-restricted helper T (Th) cells. Each of the two factors consists of two polypeptide chains, an antigen-binding chain (ABC) and a major histocompatibility complex (MHC) chain. The ABC binds LDH-B, which is then recognized by one of the two receptors of the Th cell and an antigen bridge is formed between the factor and the Th cell. This chain is presumably identical in both factors. The MHC chain of the TsF-A carries antigenic determinants recognized by three sets of monoclonal antibodies: antibodies specific for the A beta chain, antibodies specific for class II determinants expressed in T cells and controlled by the A beta-E beta chromosomal segment, and antibodies crossreacting with J determinants. The MHC chain of the TsF-E carries determinants recognized by E beta-specific and by J-specific antibodies. Only some of these serologically detectable determinants reside in the region of the TsF molecule recognized by Th cells. These findings suggest that the J determinants are carried by the modified E beta and also by the modified A beta chains.

Animals↗

Peliosis of the spleen.

Peliosis of the spleen was found in 10 out of 1,200 cases autopsied from 1977 through 1980 in our laboratory. Eight such cases had no peliosis of the liver. Histologically, it was noticed that the parafollicular areas were the most common sites of the lesions, and this feature seemed to be important for the histologic differentiation of peliosis from simple dilatation of splenic sinuses resulting from passive congestion. The clinical and anatomic features of these cases are described and previously reported cases of peliosis of the spleen are reviewed briefly.

Adolescent↗

Malignant lymphoepithelial lesion of the submandibular gland.

A case of malignant lymphoepithelial lesion affecting the submandibular gland of a 48-year-old Japanese man is described. Histologically, a well-encapsulated tumorous mass replacing almost the whole gland was composed of lymphoid and epithelial elements, and the latter revealed severe anaplasia with frequent mitotic figures indicating malignant changes. There is no sign of recurrence up to now, 32 months after the operation. Ultrastructural studies on a formalin-fixed sampling from the gland demonstrated the squamous nature of the epithelial component. This is the first case of malignant lymphoepithelial lesion of the submandibular gland detected in Japan.

Epithelium↗

Induction of T cell responses in nonresponder mice by abolishing suppression with monoclonal antibodies recognizing A region-controlled, T cell-specific determinants.

Mouse strains carrying the kappa allele at loci A beta, A alpha, E beta, and E alpha are nonresponders to lactate dehydrogenase B (LDHB) and to allotypic determinants of IgG2a myeloma proteins (for example, UPC10 used in this study). The nonresponsiveness to these antigens is caused by T suppressor (Ts) cells that prevent antigen-primed T helper (Th) cells from proliferating. We demonstrate here that monoclonal antibodies specific for an A region-controlled molecule selectively expressed on T cells (A-T) are capable of inducing anti-LDHB and anti-UPC10 responses of primed T cells from nonresponder strains. A monoclonal anti-J antibody that cross-reacts with the A-T molecule also induces responsiveness, whereas another J-specific antibody that lacks this cross-reactivity fails to do so. The mechanism of response induction is blocking of the interaction between the Ts cell or its factor (TsF) and the target of suppression, the antigen-specific Lyt-1+2- (Th) cell. The blocking occurs at the level of the Ts cell and the TsF. The data indicate that Ts cells and TsF carry a unique, A region-controlled molecule that is not only functionally analogous but also serologically similar to the J molecule.

Animals↗

[Simultaneous, bilateral hypertensive intracranial hematomas].

The reported incidences of bilateral intracerebral hemorrhages due to systemic arterial hypertension are exceptionally rare in Japan. Unilateral hemorrhages, on the other hand, are less uncommon. Recently, we have examined two patients with bilateral intracerebral hemorrhages due to hypertension. The first case involved bilateral thalamic hemorrhages; and in the other, a contralateral hemorrhage developed postoperatively, subsequent to the evacuation of a primary hematoma. The characteristic neurological manifestation of bilateral intracerebral hemorrhages include quadriparesis, bilateral Babinski's signs, stupor, and coma. Published information regarding the anatomy of intracerebral hemorrhages due to hypertension is inconclusive, but the bilateral basal ganglias are believed to be most frequently involved. One school of thought explains the pathomechanism of bilateral hemorrhages as a symmetrical rupture of cerebral microaneurysm. However, it is possible that an unilateral hematoma was formed by a ruptured microaneurysm, and subsequently, a contralateral hemorrhage developed in relatively short time due to circulatory disturbance. As in the case of general cerebral hemorrhage, a craniotomy is also indicated for hypertensive bilateral intracerebral hemorrhage.

Aged↗

Cell-to-cell interaction controlled by immunoglobulin genes. Role of Thy-1-, Lyt-1+, Ig+ (B') cell in allotype-restricted antibody production.

A novel lymphocyte subpopulation, designated "B' cell" because of its characteristic dual expression of Ig and Lyt-1 antigen, is described in relation to its ability to augment the in vitro secondary antibody response. The cells are found in the spleens of normal unprimed mice as well as those of athymic nude mice and represent a small of normal unprimed mice as well as those of athymic nude mice and represent a small number (2-3%) of immunoglobulin-positive cells. No other distinguishing surface markers of conventional T and B cells, such as Thy-1, Lyt-2, Ia, and ThB antigens, are detected on the B' cell. In the in vitro anti-hapten secondary antibody response, the addition of a small number of B' cells from unprimed mice to the mixture of T and B cells greatly augmented the anti-hapten antibody formation when the number of carrier-specific helper T cells was limited. This augmentation was observed only when B and B' cells shared the same set of IgVH genes. The identity of the immunoglobulin gene between T cells and B or B' cells was not necessary for optimum antibody production. The results indicate that the presence of B' cells is necessary for the induction of an optimum antibody response when helper T cells are limited. It is suggested that B' cells deliver an additional signal to the B cell network to magnify the antibody response.

Animals↗

Acute myelofibrosis terminating in erythroleukemic state.

A patient with acute myelofibrosis associated with erythroleukemia is described. The terminal course of the patient was marked by the erythroblast population in the peripheral blood increasing to a level of 21.8 x 10(3)/mm3, 18% of which were PAS-positive. Possible transformation of acute myelofibrosis into the erythroleukemic state is discussed.

Acute Disease↗

IgM-monoclonal gammopathy associated with malignant lymphoma with recurrent pleural effusion.

A case of malignant lymphoma (plasmacytoid lymphocytic type) with IgM-monoclonal gammopathy is presented. The main site of lesion was in the lung. The sole clinical manifestation was pleuropulmonary involvement with massive pleural effusion. A clue to the diagnosis was given by cytological and immunocytological examination of pleural aspirates. Subsequent immunological survey of serum protein and a bronchial biopsy confirmed the diagnosis.

Aged↗

Sudden death due to infantile pancreatitis.

The autopsy of a 10-month-old infant girl who died suddenly after a 2-day illness revealed acute pancreatitis and DIC. While the definitive etiology remains unknown, retention of pancreatic juice accompanying proliferation of papillary epithelium within the pancreatic duct adjacent to the ampulla Vater was suggested. Acute interstitial pancreatitis was assumed to have resulted from suppurative inflammation of the pancreatic duct. DIC was probably caused by the release of pancreatic enzymes.

Acute Disease↗