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Biomedical subjects

C Morimoto

Publications and source records attributed to C Morimoto.

263 records · Page 15Linked to original sources
PubMed1978

Cytochemical study on uptake of exogenous peroxidase by Vx2 carcinoma cells transplanted into the rabbit.

When horse-radish peroxidase (HPO) was administered iv to Vx2 carcinoma-bearing rabbits, an HPO reaction product was detected in the lumina of blood vessels and the extracellular spaces between tumor cells in the first few minutes after administration. HPO was also seen in vesicles in tumor cells. Fifteen minutes to 1 hour after administration, the HPO reaction product was found mainly in the large membrane-bound vacuoles. Within 6--12 hours, the HPO activity gradually diminished in large membrane-bound vacuoles (lysosomes). In conclusion, exogenous HPO was rapidly incorporated into Vx2 carcinoma cells by pinocytosis, and then pinocytotic vesicles were fused with lysosomes.

Animals↗
PubMed1978

Loss of suppressor T-lymphocyte function in patients with systemic lupus erythematosus (SLE).

Immunological reactivity in patients with SLE was studied in vitro trinitrobenzene sulphonate (TNP) specific antibody formation by peripheral blood lymphocytes. Lymphocytes from patients with SLE could produce an increased number of TNP-specific plaque-forming cells (PFC), while no such response could be seen in normal controls. Co-culture of lymphocytes from active SLE patients and normal controls was performed with TNP-Horse red blood cells (TNP-HRBC). The number of PFC by B lymphocytes from active SLE patients was suppressed by T lymphocytes from normal controls. On the other hand, the number of PFC by B lymphocytes from normal controls was increased by T lymphocytes from active SLE patients. Co-culture of lymphocytes from identical twins discordant for SLE was also performed, and the same results were obtained. We further examined the effects of Con A on antibody formation. Con A-treated T lymphocytes from a normal control markedly suppressed TNP-specific PFC by peripheral lymphocytes from active SLE patients. However, Con A-treated T lymphocytes from an active SLE patient did not suppress TNP-specific PFC by lymphocytes from another active SLE patient. These results suggest that active SLE patients showed a loss of suppressor T-lymphocyte function.

Adolescent↗
PubMed1977

In vitro TNP-specific antibody formation by peripheral lymphocytes from patients with systemic lupus erythematosus.

Immunological reactivity in patients with systemic lupus erythermatosus (SLE) was assessed by investigating in vitro trinitrophenyl (TNP)-specific antibody formation by peripheral lymphocytes. Peripheral lymphocytes from 16 patients with SLE were cultured with TNP conjugated with horse erythrocytes (TNP-HRBC) in the presence of 2-mercaptoethanol. The hemolytic plaque assay was used to detect hapten (TNP)-specific antibody-forming cells. Peripheral lymphocytes from normal individuals failed to produce antibody to TNP, whereas SLE lymphocytes produced a significant number of plaque-forming cells. Co-culture experiments with SLE and normal lymphocytes suggested that patients with SLE have a defect in T lymphocytes, leading to abnormal antibody production.

Adolescent↗
PubMedDate not supplied

Propranolol-sensitive binding of lipolytic agents to lipid droplets from adipocytes.

We established a cell-free system in which epinephrine and other lipolytic agents stimulated lipolysis of endogenous lipid droplets from fat cells by hormone-sensitive lipase. The endogenous lipid droplets were prepared by hypotonic treatment of fat cells and their successive washing with buffer containing 0.025% Triton X-100. In the cell-free system, propranolol inhibited lipolysis induced by various lipolytic agents such as norepinephrine, theophylline and cyclic AMP (cAMP), whereas phenoxybenzamine did not inhibit lipolysis. The binding of these lipolytic agents to endogenous lipid droplets was inhibited by propranolol, but not by phenoxybenzamine. The "propranolol-sensitive" binding of these lipolytic agents to the droplets may be involved in lipolysis. Treatment of the droplets with phospholipase C, but not phospholipase D, inhibited the propranolol-sensitive binding of these lipolytic agents to the droplets. These results suggest that the phosphate group of phospholipid in the droplets may be the site of propranolol-sensitive of binding of theophylline, and cAMP in addition to norepinephrine.

Adipose Tissue↗
PubMedDate not supplied

A novel epitope of the LFA-1 antigen which can distinguish killer effector and suppressor cells in human CD8 cells.

The CD4 subset of cells displays helper/inducer activity and recognizes class II antigens of the major histocompatibility complex (MHC), while the CD8 subset recognizes class I MHC antigens and exhibits cytotoxic or suppressor function. Considerable functional as well as corresponding phenotypic heterogeneity exists within the two major T cell subsets. Although the CD8+ population contains pre-cytotoxic, cytotoxic, pre-suppressor and suppressor effector T cells, these distinctions still rest largely on the use of functional assays. Attempts have been made to define the CD8+ precursor of the killer cell with new monoclonal antibodies. But more precise phenotypic distinctions between the functional subpopulations within CD8+ cells will be needed. We have now developed a monoclonal antibody, anti-S6F1 which can distinguish killer effector and suppressor effector cells in CD8 lymphocyte populations. The cell-surface structure defined by this antibody comprises two glycoproteins with relative molecular mass (Mr) 180K and 95K respectively. Also sequential immunoprecipitation studies and two dimensional gel electrophoresis indicate that anti-S6F1 recognizes a novel epitope on the LFA-1 antigen.

Animals↗
PubMedDate not supplied

Rapid inhibitory effect of tacrolimus on T cell migration by suppressing CD29-related functions.

OBJECTIVE: To clarify the direct effect of Tacrolimus (FK506) on T cell function in relation to CD29. METHODS: Human T cell line H9 and phytohemagglutinin (PHA)-activated T cells were incubated with or without Tacrolimus. The cells underwent cell migration assay by using fibronectin-coated trans-wells, and at the same time the degree of adherence by cultured cells to fibronectin-coated plastic wells was measured. For H9 cells, intracellular filamentous actin formation and the cell surface expression of CD3, CD11a, CD25, CD26, CD44, CD29 were measured by using flow cytometry. Intracellular tyrosin-phosphorylation induced by fibronectin by CD29 stimulation in H9 cells was analyzed by immunoblotting. RESULTS: The ability of H9 cells and PHA-activated T cells incubated with Tacrolimus for 2 hours (hrs) to migrate and to adhere to fibronectin was significantly suppressed. However, the inhibiton was transient, because the ability of cells incubated with Tacrolimus for 24 hrs to migrate was not affected despite the suppression of cell replication. Tacrolimus showed slight but significant reduction of cell surface expression of CD29 within 4 hrs, but CD3, CD11a, CD25, CD26 and CD44 were not affected. Tacrolimus rapidly inhibited intracellular filamentous actin formation; the maximum inhibition was within 2 hrs and the effect was not observed at 6 hrs. Intracellular tyrosin-phosphorylation induced by CD29 stimulation was also inhibited by, Tacrolimus in H9 cells. CONCLUSION: Tacrolimus appeared to have transient early phase inhibitory effects on CD29-related function that may be associated with T cell migration.

Cell Adhesion↗
PubMedDate not supplied

Characterization of the CD8+CD45R+(2H4+) suppressor effector cell.

In the present study, we have investigated the molecular basis for immunoregulatory function of CD8 cells after autologous mixed lymphocyte reaction (AMLR) activation. We demonstrated that the CD8+CD45R+ but not the CD8+CD45R- subset of cells was a subpopulation, with the majority of suppressor activity after AMLR activation. In contrast, cytotoxic activity against alloantigens resided in both the CD8+CD45R+ and CD8+CD45R- subsets of cells. Importantly, the treatment of AMLR-activated CD8 cells with anti-CD45R antibody or anti-CD3 antibody abolished the suppressor function of these cells, which contrasts with earlier studies showing that treatment of AMLR activated CD4 suppressor inducer cells could be blocked with anti-CD45R but not with anti-CD3 antibody. The results suggest that the CD45R antigen as well as the CD3-T cell receptor (TCR) complex have an important role in the suppressor function of AMLR-activated cells.

Antigens, CD↗
PubMedDate not supplied

P. Rambotti Lecture. Human naive and memory T cells revisited: new markers (CD31 and CD27) that help define CD4+ T cell subsets.

The human CD4 population can be divided into functionally distinct and largely reciprocal subsets based on their differential expression of CD45 isoforms (CD45RA, CD45RO) and the CD29/VLA beta chain. CD4+CD45RO+ CD29high "memory" (helper inducer) cells respond maximally to recall antigens and provide help for B cell IgG synthesis. In contrast, the CD4+CD45RA+ CD29low "naive" (suppressor inducer) population responds poorly to recall Ag, lacks helper function for B cells, but can both induce CD8 cells to suppress B cell IgG synthesis and proliferate preferentially in an autologous mixed lymphocyte response (AMLR). The phenotypic "conversion" after activation and the preferential responsiveness of CD45RA-CD45RO+ CD29high cells to recall antigen led to the view that CD45RA+ cells are "naive" and immature and convert to CD45RA-CD45RO+ "memory" cells after activation. This conversion was believed by many to be unidirectional and irreversible. It has become increasingly clear that the naive-memory concept outlined above is far from settled and that naive CD4+CD45RA+ T cells retain their unique functional program after activation and are distinct from the freshly isolated CD4+CD45RO+ subset. Moreover, CD45RA is not irreversibly lost following activation, but in fact recycles on the cell surface. Given the problems with CD45 isoform expression as a definition of maturational state, we have investigated the possibility that more reliable cell surface molecules are needed which could delineate between the functions of activated CD45RA+ and CD45RA- CD45RO+ cells. We could show that CD31 and CD27 are preferentially expressed on the CD4+CD45RA+ subset of cells and their expressions are stably maintained on these cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, CD↗