Relative rates of photo-excited quinones for the reaction with isopropyl alcohol.
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Alcohols↗
Biomedical subjects
T Hamaoka
Publications and source records attributed to T Hamaoka.
Antibody response of the tumor-bearing animals.
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Amylases↗
CCK pathway from supramammillary region to the nucleus anterior ventralis thalami of the young rats.
The existence of cholecystokinin-8-like immunoreactive (CCKI) pathway from supramammillary region (SUM) to the nucleus anterior ventralis thalami (AVT) was demonstrated in this study by means of experimental immunohistochemical manipulations in very young rats, because destruction of unilateral SUM, which contains CCKI neurons, resulted in a disappearance of CCKI fibers in the ipsilateral AVT.
Animals↗
A sequence of cellular and molecular events involved in IL12-induced tumour regression.
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Animals↗
Mouse CD4 and CD8 T-cell clones that recognize xeno-antigens directly on xeno-antigen presenting cells in xeno MHC-restricted ways.
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Animals↗
Tumor vaccination that enhances antitumor T-cell responses does not inhibit the growth of established tumors even in combination with interleukin-12 treatment: the importance of inducing intratumoral T-cell migration.
Interleukin-12 (IL-12) treatment is effective in the CSA1M but not in the Meth A and CSA1M-variant tumor models. The authors investigated the cause by which IL-12 treatment fails to induce tumor regression in these two tumor models. T cells from CSA1M-bearing mice have high levels of IL-12 responsiveness, whereas cells from Meth A-bearing mice display marginal levels of responsiveness. Because IL-12 responsiveness in T cells is induced after T-cell receptor stimulation, the lack of IL-12 responsiveness suggests that T cells in Meth A-bearing mice are not sensitized to Meth A tumor antigen. Immunization of normal mice with attenuated Meth A tumor cells resulted in a protective immunity, as shown by the rejection of challenged viable Meth A cells. Such an immunization, when performed in Meth A-bearing mice, induced potent IL-12 responsiveness in T cells. Nevertheless, IL-12 treatment in these mice did not inhibit tumor growth. In another IL-12-incurable (CSA1M-variant) model, IL-12 responsiveness was observed before tumor cell immunization. However, IL-12 treatment was ineffective regardless of whether tumor cell immunization was performed. In these two models, the failure of IL-12 treatment to induce tumor regression was associated with the lack of T-cell migration to tumor sites. These results indicate that the sensitization of T cells to tumor antigens and generation of IL-12 responsiveness are insufficient to induce tumor regression when these sensitized T cells are not allowed to migrate to tumor sites.
Animals↗
Proliferation and differentiation of immature thymocytes induced by a thymic stromal cell clone.
The monolayer of our established thymic stromal cell clone (MRL104.8a) exhibited the capacity to maintain immature double-negative thymocytes. Such capacity was also expressed by a factor produced by the MRL104.8a monolayer. This factor designated as thymic stroma-derived T cell growth factor (TSTGF) was found to be distinct from IL-2 or IL-4 but similar to IL-7 of the previously described cytokines from the functional and molecular aspects. The MRL104.8a monolayer also exerted its differentiation-promoting effect on double-negative thymocytes. Culture for one day of purified double-negative thymocytes on the monolayer resulted in the induction of an appreciable per cent of CD3-4-8+ cells. This differentiation could also be induced by a semipurified TSTGF sample but not by recombinant IL-7, suggesting that the MRL104.8a cells elaborate a factor(s) responsible for initiating the differentiation of double-negative cells in addition to the growth-promotion factor identical or closely related to IL-7. When the culture period of double-negative thymocytes was extended to 2 or 3 days, an appreciable number of double-positive (CD4+8+) and single-positive (CD4+8-) cells were generated on the MRL104.8a monolayer. Thus, these observations provide strong support for the proposition that a specialized thymic stromal component plays an essential role in the intrathymic T cell development in the context of T cell growth and differentiation.
Animals↗
Autoimmune thyroiditis induced in mice depleted of particular T cell subsets. II. Immunohistochemical studies on the thyroiditis lesion.
The intravenous (i.v.) administration of Lyt-1dull T cells into syngeneic (C57BL/6 x C3H/He)F1 T cell-depleted B cell mice resulted in the induction of typical thyroiditis exhibiting massive cellular infiltration. The present study investigated which types of lymphoid cells infiltrate in the thyroiditis lesion and whether immunohistologic change takes place on epithelial cells of thyroid follicles. Both L3T4+ and Lyt-2+ T cells were found in the lesion, although the frequency of infiltration was higher in the former than in the latter. Thyroiditis was also induced by injection of Lyt-1dull L3T4+ but not of Lyt-1dull Lyt2+ T cells, indicating the critical role of a part of L3T4+ T cell subset (Lyt-1dull L3T4+ T cell subpopulation) in inducing thyroiditis. Only rare Lyt-2+ T cells were seen in such a thyroiditis lesion. Infiltrating T cells were predominantly of L3T4+, and these L3T4+ T cells formed cellular infiltrating lesion together with moderate number of B cells and relatively small number of macrophages. Importantly, class II MHC antigens were detected on epithelial cells of thyroid follicles. Such class II MHC expression was observed in coincidence with the area of cellular infiltration in the thyroid. These results demonstrate that: (1) a part of L3T4+ T cells which is required for the induction of thyroiditis by adoptive cell transfer infiltrates into the inflammatory lesion, (2) the induction of the thyroiditis lesion is formed by these L3T4+ T cells as well as B cells and macrophages, but does not necessarily depend on the participation of Lyt-2+ T cell subset, and (3) the aberrant expression of class II MHC antigens on thyroid epithelial cells coincides with cellular infiltration.
Animals↗
Type II collagen-induced murine arthritis. II. Genetic control of arthritis induction is expressed on L3T4+ T cells required for humoral as well as cell-mediated immune responses to type II collagen.
The present study investigates the cellular and molecular mechanisms responsible for expressing genetic control of type II collagen-induced murine chronic arthritis. Analyses were made for both humoral and cellular immune responses, since the induction of arthritis required synergy between both types of immunities. Immunization of high (DBA/1) and low (C57BL/6, C3H/He, BALB/c) responder mice with native bovine type II collagen resulted in the production of the respective high and low levels of anti-collagen antibody. However, polyclonal in vitro stimulation of normal spleen cells from high or low responder mice with lipopolysaccharide (LPS) induced a comparable magnitude of anti-collagen antibody responses, indicating the localization of the genetic defect at cellular levels other than B cells themselves. In contrast to immunization with native collagen, sensitization of DBA/1 mice with heat-denatured collagen failed to stimulate B cells, but resulted in selective generation of L3T4+ T cell-mediated immunity. These included anti-collagen delayed-type-hypersensitivity (DTH) responses and the generation of various interleukins (IL) responsible for antibody production as well as DTH responses. It was demonstrated that there was appreciable difference in the magnitudes of these responses between lymphoid cells from high and low responder mice. Differential effects of sensitization with heat-denatured collagen in high versus low responders were reflected on the genetic difference in the development of chronic arthritis. A typical arthritis was induced neither in denatured collagen-sensitized DBA/1 mice nor in unsensitized mice transferred with anti-collagen antiserum. However, the antiserum transfer into denatured collagen-sensitized DBA/1 mice induced chronic perpetuating arthritis. This sharply contrasted with the failure of the same aliquot of the antiserum to induce a chronic arthritis when inoculated into denatured collagen-sensitized low responder mice. These results indicate that the genetic control of the induction of arthritis is expressed on L3T4+ T cells which are required for generating anti-collagen humoral as well as cell-mediated immunities as assessed by DTH responses in vivo or lymphokine productions in vitro.
Animals↗
Prevention of suppression of alloreactive capacity following intravenous injection of neuraminidase-treated allogeneic cells by co-injection of agents competing for asialoglycoprotein receptor.
Intravenous (i.v.) administration of neuraminidase (Nase)-treated allogeneic lymphocytes resulted in the complete abrogation of the capacity to develop delayed-type hypersensitivity (DTH) responses to the relevant alloantigens (tolerance induction). The Nase treatment did not influence the antigenicity of allogeneic lymphocytes, as subcutaneous inoculation of Nase-treated cells was capable of generating comparable anti-allo-DTH responses to those induced by untreated allogeneic cells. However, Nase-treated lymphocytes were revealed to exhibit strikingly enhanced reactivity to the lectin peanut agglutinin (PNA) as well as adhesion to hepatocytes in the primary culture. Such enhanced PNA-reactivity was inhibited by lactose but not by maltose, and enhanced hepatocyte-adhesion was also inhibited by N-acetyl-galactosamine (GalNAc) but not by N-acetyl-glucosamine (GlcNAc), indicating augmented reactivity of Nase-treated cells to Gal/GalNAc-specific receptors on hepatocytes. It was also demonstrated that i.v. infusion of Nase-treated, 51Cr-labeled lymphocytes leads to an increased radioactivity in the liver and that this enhanced retention of radioactivity can be inhibited by the co-injection of Nase-treated, unlabeled syngeneic erythrocytes. Most importantly, the co-injection of Nase-treated allogeneic lymphocytes and Nase-treated erythrocytes resulted in the prevention of the suppression of anti-allo-DTH responses as induced by the injection of Nase-treated allogeneic cells alone. These results indicate that Nase-treated allogeneic cells are entrapped in the liver in a strikingly increased way through their enhanced reactivity to Gal/GAlNAc receptor of the liver and suggest that such enhanced entrapment by the liver has a crucial role in inducing anti-allo-DTH tolerance.
Animals↗
The suppressive effect of antibodies on cellular cooperation.
1) The primary and secondary anti-carrier antibody responses were markedly suppressed by the passively administered anti-carrier antibody but not by the anti-hapten antibody. 2) The primary and secondary anti-hapten antibody responses were suppressed not only by the passively administered anti-hapten antibody but also by the anti-carrier antibody. 3) Passively administered 3.5S fragments of the anti-carrier antibody selectively suppressed the anti-carrier antibody response but had no effect on the capacity of carrier-specific helper T cells to facilitate the anti-hapten antibody response. 4) Passively administered anti-carrier antibodies did not suppress the development of carrier-specific helper T cells but suppressed B memory cells specific for the haptenic group as well as the carrier determinant.
Amylases↗
Thymic stromal cells eliminate T cells stimulated with antigen plus stromal Ia molecules through their cross-talk involving the production of interferon-gamma and nitric oxide.
We previously established a thymic stromal cell clone capable of inducing differentiation of immature thymocytes and described a clonal elimination model in which T cell clones are killed on the monolayer of this stromal clone by stimulation of their T cell receptors (TCR) with antigen plus stromal Ia molecules. This study investigated molecular mechanisms underlying this phenomenon. Antigenic stimulation on thymic stromal cells produced large amounts of interferon-gamma (IFN-gamma) and small amounts of tumor necrosis factor-alpha (TNF-alpha). Addition of anti-IFN-gamma monoclonal antibody (mAb) to these cultures largely prevented death of TCR-stimulated T cells. T cell death was also induced when cultures were treated with recombinant IFN-gamma (rIFN-gamma) or rTNF-alpha instead of the relevant antigen, showing that these lymphokines are involved in the process of T cell death. It was further demonstrated that these lymphokines, especially IFN-gamma, induced the expression of mRNA for the inducible type of nitric oxide (NO) synthase in thymic stromal cells and that enhanced levels of NO were produced by stromal cells cultures with T cells plus antigen or stimulated with rIFN-gamma or rTNF-alpha. NO was found to be critically responsible for inducing T cell death on the stromal cell monolayer following stimulation of T cells with antigen or of stromal cells with rIFN-gamma or rTNF-alpha, because T cells death was completely prevented by addition of NG-monomethyl-L-arginine (L-NMMA), which is capable of inhibiting NO production. These results indicate that elimination of TCR-stimulated T cells on thymic stromal monolayers with the capacity to support thymocyte differentiation is induced by the cross-talk between IFN-gamma/TNF-alpha-producing T cells and stromal cells capable of producing NO in response to these lymphokines.
Cell Communication↗