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T Tada

Publications and source records attributed to T Tada.

At least 361 records · Page 20Linked to original sources
PubMed1985

Human ductus arteriosus. A histological study on the relation between ductal maturation and gestational age.

The present study deals mainly with the ductus arteriosus of preterm infants of gestational age less than 29 weeks, birth weight less than 1200 g, and postnatal age less than 72 hours. Excised ductus were histologically examined postmortem and compared to those of infants of more advanced gestational age. Intimal cushion and duplication and/or interruption of the internal elastic lamina of the ductus arteriosus were employed as the indicators of the maturation of the ductus arteriosus. The ductus arteriosus of infants with gestational age more than 29 weeks showed histologically more mature features than those of 28 weeks or less. It is considered that there is a relation between gestational age and histologic maturation of the ductus arteriosus.

Aorta↗
PubMed1985

[A case of multiple cavernous hemangiomas of the lung].

A case of multiple cavernous hemangiomas of the lung is presented. A 61-year-old woman was suffering from mitral stenosis and insufficiency. On the chest roentgenogram, multiple tumor shadows were revealed at all the lobes of the lung. She had been followed up for about 10 years under the diagnosis of the metastatic carcinoma of the lung. But no tumor lesion had been found at any other organs. Throughout this period, the tumor shadows had not changed in size or number. She died of congestive heart failure, and an autopsy was performed. Histologically, the tumors were diagnosed as cavernous hemangiomas and differentiated from arteriovenous fistula or sclerosing hemangioma.

Female↗
PubMed1984

Heterogeneity of Igh-linked allotypic determinants expressed on functional T cell subsets as detected by monoclonal antibodies.

Hybridomas producing monoclonal antibodies (mAb) specific for immunoglobulin heavy chain (Igh) allotype-linked gene products expressed only on functional T cells but not on B cells and macrophages were established by fusion of allotype congenic SJL (Igh-1b) and SJA /9 (Igh-1a) B cells immunized reciprocally with partner spleen cells with a myeloma P3-X63-Ag8-653 of BALB/c origin. Nine mAb have been selected on the criteria that they can specifically block various antigen-dependent functions of known T cell subsets in in vitro immune responses of mouse strains having the corresponding Igh allotype, but not the other one. These included (a) four mAb that augment the in vitro secondary antibody response of either Igh-1a or Igh-1b strains and thus are considered to react with the Igh-linked allotypic determinant expressed on suppressor T cells, (b) one mAb that inhibits the helper T cell activity of Igh-1b but not of Igh-1a strains, (c) two mAb that inhibit the antigen-induced proliferative response of Igh-1a but not Igh-1b strains, and (d) two mAb that block the cytotoxicity of alloreactive cytotoxic T cells of Igh-1a strains. The linkage to Igh-1 allotype of the T cell products was established by testing with Igh-1-congenic strains with different backgrounds including the H-2 complex. Some of the mAb were able to react with cloned hybridomas and a continuous cell line of the given allotype and functions. Each mAb was able to block one of the known functions of T cell subsets, but not others, indicating the existence of the heterogeneity and multiplicity of the Igh allotype-linked products on T cells.

Animals↗
PubMed1984

Photoaffinity-labeled hapten-binding T-cell receptor on a suppressor T-cell hybridoma.

A T-cell hydridoma, 7C3-13-Ag6, which produces a (4-hydroxy-3-nitrophenyl)acetyl (NP)-specific suppressor T-cell factor associated with an I-J determinant, was utilized to study the hapten-binding receptor of T-cells. This hybridoma had been shown to express NP-binding receptor molecules on the cell surface with heteroclitic fine specificity for a cross-reactive hapten, (4-hydroxy-5-iodo-3-nitrophenyl) acetyl (NIP). The stoichiometric analysis of the hapten binding by 7C3-13-Ag6 cells was performed by the measurement of direct binding of highly radioactive haptens to the cell surface. The affinity constant (Ka) of the receptor for N125IP-epsilon-aminocaproic acid (N125IP-cap), as calculated from a Hill plot, was 5.75 X 10(7) M-1 [Hill coefficient (a) = 0.86; expression of receptor sites per cell = approximately 1 X 10(3) on average]. The receptor molecule was specifically affinity labeled with photoreactive nitroaryl azide derivatives of N125IP (510-570 Ci/mmole). The specificity of photoaffinity labeling was demonstrated both by competitive inhibition of labeling with NIP- or NP-cap and by differential photoaffinity labeling based on the reversibility of hapten-receptor interaction. The gel electrophoretic analysis of the photoaffinity-labeled molecule indicated that the hapten-binding receptor of 7C3-13-Ag6 has a mol. wt of 28,000 +/- 3000 and an isoelectric point of 5.6-5.7. No immunoglobulin determinants were detected on the molecule. A comparative immunoprecipitation analysis of the membrane lysate of 7C3-13-Ag6 with monoclonal anti-I-J reagents identified a separate I-J molecule of 25,000 +/- 1000 mol. wt that is distinct from the photoaffinity-labeled hapten-binding molecule.

Affinity Labels↗
PubMed1984

High incidence of peliosis hepatis in autopsy cases of aplastic anemia with special reference to anabolic steroid therapy.

The livers were collected from 47 autopsy cases of aplastic anemia aiming to study the correlation between the use of androgenic anabolic steroid and the formation of peliosis hepatis. Association of peliosis hepatis was found in 7 cases out of 19 cases with anabolic steroid therapy, while peliotic cavities were found only in one case out of the remaining 28 cases without anabolic steroid therapy. Out of 7 cases specified above, peliotic cavities in 5 cases were phlebectatic; phlebectatic and parenchymal types of peliotic cavities coexisted in one case, and one case was parenchymatous. Besides these cavity formations, remarkable dilatation of sinusoids often distinct at the periphery of the hepatic lobule was found in the 7 cases.

Adolescent↗
PubMed1984

Transduction of effector-suppressor T cells by an antigen-specific suppressor T cell factor and Lyt-1+,2+,3+ T cells.

The cellular consequences in the suppression of IgG antibody formation initiated by an antigen-specific suppressor T cell factor (TsF) were investigated. The initial step of the suppression is the production of TsF by Lyt-2+,3+ T cells (Tsi) which activates Lyt-1+,2+,3+ acceptor T cells in the nylon wool-adherent T cell population. The activated Lyt-1+,2+,3+ T cells further generate a new effector-suppressor T cell ( Tse ) that belongs to the Lyt-2+,3+ T cell subset in the culture of nylon-adherent T cells with antigen. The Tse thus induced directly suppresses the responses mounted by B cells and nylon column-purified helper T cells in the absence of TsF. The origin of Tse was further examined by utilizing Lyt congeneic mice. The result indicates that Lyt-1+,2+,3+ acceptor T cells themselves do not differentiate into Lyt-2+,3+ Tse with losing Lyt-1 phenotype but facilitate the transduction of Tse from a preexisting precursor pool. These cellular interactions strongly suggest that Lyt-1+,2+,3+ T cells play a decisive role in an amplification of immunoregulation.

Animals↗
PubMed1984

Regulation of allotype-linked NPb idiotype by an idiotype-positive soluble factor derived from a T cell hybridoma. Coupling of the circuit regulation to the network concept.

We reported in this paper genetic requirements for the suppression of anti-4-hydroxy-3-nitrophenylacetyl (NP) antibody response induced by an NP-specific, Igh-1 linked idiotype (NPb) positive T suppressor factor (NPb-TsF) derived from a T cell hybridoma 7C3-13 of B10.BR (Igh-1b, H-2k) mouse origin. NPb-TsF could suppress the responses mounted by primed spleen cells of all IgVH compatible strains regardless of their H-2 haplotypes. The majority of the anti-NP antibody response suppressed by NPb-TsF was idiotype positive (Id+). NPb-TsF was also capable of suppressing the responses of H-2 compatible but Igh incompatible strains where responding cells do not produce NPb idiotype. NPb-TsF was incapable of suppressing the responses of mouse strains who are incompatible both in IgVH and H-2 loci, indicating that the identity in either IgVH or H-2 genes between NPb-TsF and responding cells was necessary for the initiation of the suppression by NPb-TsF. It was further found that the NPb-TsF utilizes anti-idiotypic Lyt-1+2+3+ T cells (transducer cells), which are present only in IgVH compatible strains, to ultimately suppress the Id+ antibody production by B cells. These results indicate that there exists a pathway where an idiotypic NPb-TsF activates a suppressor circuit mediated via the idiotype-antiidiotype interactions apart from the previously described carrier-specific and H-2 restricted suppressor circuit. Both pathways involve the 'transduction' step utilizing Lyt-1+2+3+ intermediary T cells. Our experiments provide important clues for coupling the two major immunological concepts, network and circuit.

Animals↗
PubMed1984

Is there multiplicity in I-J subregion products?

Recent studies in molecular genetics have revealed the striking fact that the previously known I-J subregion (or I-J gene) does not exist at the exactly prescribed position in the I-region of the murine major histocompatibility complex (MHC). How, then, can we comprehend the established serological and functional significance of I-J genes and I-J products? To answer this question we reexamined systematically the specificities and functional activities of monoclonal anti-I-J antibodies. A series of monoclonal anti-I-Jk antibodies were newly established by fusion of B10.A(3R) spleen cells immune to B10.A(5R) lymphoid cells with P3X63-Ag8-653. Their abilities to eliminate known functions of T cell subsets and to react with I-J+ T cell clones of defined functions were examined in an in vitro secondary antibody response and by fluorescence-activated cell sorter analysis. The monoclonal antibodies (mAb) were divided into three groups: (1) those reactive with suppressor inducer T cells (Tsi), Tsi hybridomas, and the antigen-specific T cell factor (TsF) derived from them; (2) those specific for suppressor effector T cells (Tse) and Tse clones; and (3) those reactive with some but not all helper T cells. The determinants detected by these three different groups of antibodies are apparently present on separate, nonoverlapping cell populations and functionally distinct clones. The above results indicate the multiplicity of I-J products expressed on different T cell subsets, and sharply contradict the notion, derived from molecular genetics, that not even a single gene can be accommodated in the I-J subregion. To resolve this dilemma, we compared the above results with those obtained with another set of mAb that also detected I-region-controlled determinants on augmenting and helper T cells. Although the specificities of these mAb clearly mapped to within the I-region, none of them reacted with conventional class II Ia antigens of B cells and macrophages. The common properties shared by these anti-Ik and anti-I-Jk antibodies are that (1) they react only with T cells and T cell clones with I-region-controlled functions; (2) they can block some of the Ia-restricted cell interactions, including those of helper and suppressor T cells; and (3) they inhibit the syngeneic and/or allogeneic mixed lymphocyte reaction (MLR) by blocking the responder but not the stimulator cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Establishment and functional analysis of a cloned, antigen-specific suppressor effector T cell line.

A long-term cultured suppressor T cell line (3D10) was established from the spleen cells of KLH hyperimmunized C3H mice. The cells of 3D10 suppressed the secondary antibody response against dinitrophenylated KLH both in vitro and in vivo. The 3D10 cells were capable of directly suppressing the antibody response mounted by B cells and Lyt-1+2-helper T cells without participation of Lyt-1+2+ cells, which indicates that 3D10 is an effector rather than an inducer-type suppressor T cell. The cell line was unable to suppress the response against DNP-FGG even in the presence of free KLH. By analysis with a fluorescence-activated cell sorter, 3D10 was found to bear determinants detectable by conventional anti-Ia as well as rabbit anti-VH. The Ia locus was mapped in the I-J subregion and was detected by either conventional or monoclonal anti-I-J antibodies. The I-J determinants detected by monoclonal antibodies were different from those expressed on inducer-type suppressor T cells. The cell line also bears an antigenic determinant detected by a monoclonal SJL anti-SJA/9 antibody (HA16) that recognizes an allotypic determinant on T cells linked to the immunoglobulin heavy chain locus. The results indicate that the cell line 3D10 represents a suppressor effector T cell that acts directly on carrier-specific helper T cells.

Animals↗
PubMed1984

Characterization of an antigen-specific suppressive factor derived from a cloned suppressor effector T cell line.

A cloned effector-type suppressor T cell line, 3D10, which is known to suppress the antibody response against dinitrophenylated keyhole limpet hemocyanin (KLH), produced a soluble KLH-specific factor (TsF) that can replace the function of parental T cell clones. High activity of TsF was released spontaneously into the culture supernatant when cultured in interleukin 2 (IL 2)-containing medium, requiring no antigenic stimulation. The culture supernatant of 3D10 was also capable of inhibiting the KLH-induced proliferative response of primed T cells in an antigen-specific manner. The direct target of TsF was found to be Lyt-1+2- T cells undergoing an early stage of antigen-specific proliferation. TsF was antigen binding but lacked any other serologic markers such as I-J and immunoglobulin heavy chain-linked allotypic determinants on T cells. No genetic restriction was found in its action on allogeneic T cells. The production of IL 2 in proliferative T cells by antigenic stimulation was not inhibited by TsF. These results indicate that the TsF described here is the legitimate mediator produced by the effector-type suppressor T cell that suppresses the antigen-specific responses of Lyt-1+2- T cells. The m.w. of TsF was approximately 75,000.

Animals↗
PubMed1983

Monoclonal suppressor factor specific for lactate dehydrogenase B. I. Mechanism of interaction between the factor and its target cells.

Hybridomas secreting a monoclonal T suppressor-effector factor (TseF) were produced by fusion of a lactate dehydrogenase B (LDHB)-specific long-term T suppressor-effector (Tse) cell line with the BW5147 thymoma. A short exposure (4 h) to TseF completely suppresses the antigen-specific and A-restricted proliferation of LDHB-primed Lyt-1+2- [possibly helper (Th)] cells. The action of TseF on Th cells, as that of the Tse cells themselves, is antigen-specific and A-restricted. The interaction of TseF with Th cells involves two binding events, of which one occurs via antigen bridge, and the other represents the recognition of a factor-derived Ak-like moiety by the anti-Ak receptor of Th cells. The Ak-like moiety of the TseF carries the determinants that serve as restriction elements for antigen recognition by Th cells, and additional determinants demonstrable by T cell-specific monoclonal "anti-Ak" antibodies, however, it lacks serologically detectable determinants of the B cell-derived A alpha A beta class II Mhc molecules.

Animals↗
PubMed1983

Presence of IgT-C and I-A subregion-encoded determinants on distinct chains of monoclonal antigen-specific augmenting factor derived from a T cell hybridoma.

Monoclonal antibodies specific for mouse T cell alloantigens, Tindd and Tsud, linked to the Igh-1 locus on chromosome 12, were used to directly define the antigen-binding molecule produced by a cloned hybridoma. The T cell hybridoma, FL10, was established from antigen-binding T cells of A/J mice. FL10 produces an antigen-specific augmenting T cell factor (TaF) that bears a unique I region-controlled determinant (I-A) and has antigen-binding capacity. The Tindd, but not the Tsud, determinant was detected on the surface of FL10. The presence of both Tindd and I-A subregion-controlled determinants on FL10-derived TaF was directly demonstrated by the adsorption of TaF with immunoadsorbents prepared with monoclonal antibodies. The Igh-1-linked T cell alloantigen, Tsud, was not found on TaF. Further experiments indicated that Tindd is present on the antigen-binding polypeptide chain and not on the second chain bearing the I-A determinant. Despite the presence of the Tindd determinant on hybridoma-derived TaF, augmentation induced by TaF was restricted by the H-2 type of the responding mice and not by the Igh-1 allotype.

Animals↗