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M Hirashima

Publications and source records attributed to M Hirashima.

100 records · Page 6Linked to original sources
PubMed1980

Regulatory role of IgE-binding factors from rat T lymphocytes. IV. Formation of IgE-binding factors in rats treated with complete Freund's adjuvant.

Mesenteric lymph node (MLN) cells from rats treated with complete Freund's adjuvant (CFA) spontaneously released soluble factors, which have affinity for IgE (IgE-binding factors). The factors were purified by absorption of culture filtrates of the lymphocytes with IgE-Sepharose followed by elution at acid pH. Purified IgE-binding factors selectively suppressed IgE-forming cell response of DNP-ovalbumin-primed MLN cells to homologous antigen without affecting the IgG2 response. Fractionation of purified IgE-binding factors on lentil lectin-Sepharose showed that the majority of IgE-binding factors did not have affinity for lentil lectin, whereas a minor fraction was bound to the lectin-coupled beads. It was found that IgE-binding factors lacking affinity for lentil lectin suppressed IgE response, whereas those eluted from lentil lectin-Sepharose selectively enhanced IgE response. Serum of CFA-treated animals also contained both IgE-suppressive factor and IgE-potentiating factor, and the amount of the former factor was more than the latter. The source of IgE-suppressive factor is non-B lymphocytes. Depletion of Fc, receptor(+) lymphocytes in MLN cells from CFA-treated animals did not affect the formation of IgE-suppressive factor, indicating that Fc epsilon R-bearing cells are not the source of the factor.

Animals↗
PubMed1978

A macrophage chemotactic factor sharing common antigenicity with immunoglobulin G from DNP-ascaris extract-induced skin lesion in guinea-pig.

A macrophage chemotactic factor (factor a) was extracted from DNP-ascaris extract-induced skin lesions (showing a maximal macrophage reaction) in guinea-pigs and then purified by gel filtration on Sephadex G-100 and chromatography using DEAE-Sephadex and CM-Sephadex. This material was a thermolabile protein (free of nucleic acid) with a molecular weight of about 150,000. It shared commom antigenicity with serum IgG, and its chemotactic acitivity was completely absorbed by anti-IgG and anti-light chain antibodies, but not by anti-BSA antibody. In contrast to leucoegresin, this material seemed active for macrophages but not for neutrophils. Less active factors b and c were thermostable and not absorbed by the antibodies described above. The ratio of chemotactic activity of factors a, b and c in the skin extracts was roughly 60:25:15.

Animals↗
PubMed1978

The mediation of macrophage reaction in inflammation, with special reference to IgG-derived chemotactic factor.

Three different macrophage chemotactic factors were separated from hypersensitivity skin lesions induced by DNP-ascaris extract or PPD. The amount of each factor seemed to be changeable according to the nature of inflammatory stimuli. The chemotactic activity of the factor a was completely absorbed by anti-IgG and anti-light chain antibodies, while that of the factors b and c was not absorbed by the antibodies. The factor a was produced from IgG by neutrophil neutral serine protease resembling elastase but failing to digest elastin-orcein; its chemotactic generation was accompanied by release of dialysable peptide(s) from the IgG molecule, suggesting a minor structural change of the IgG molecule. Production of leucoegresin or lymphocyte chemotactic factor by neutrophil neutral thiol protease from IgG molecule was discussed.

Animals↗
PubMed1976

The mediation of tissue eosinophilia in hypersensitivity reaction. I. Isolation of two different chemotactic factors from DNP-Ascaris extract-induced skin lesion in guinea-pig.

In an active cutaneous anaphylaxis induced by DNP-ascaris extract in guinea-pig, tissue eosinophilia manifested two phases; the early and mild phase became maximal in about 6 h, while the delayed and intense phase in 18-24 h. Skin extracts from the lesions exhibited chemotactic activities for eosinophils, respectively comparable to the intensity of tissue eosinophilia in each phase; and two different chemotactic factors for eosinophils of skin extracts were separated by gel filtration on Sephadex G-100. The mediation of the early phase seemed to be associated with a thermostable factor with amolefular weight of less than 1400; this factor seemed to be related to mast cell degranulation. The mediation of the delayed phase appeared to be associated with a thermolabile factor with a molecular weight of about 70,000, probably independent of mast cell degranulation; the factor was considered to be more significant than the thermostable factor, because the delayed tissue eosinophilia was more intense than the early tissue eosinophilia.

Anaphylaxis↗
PubMed1976

The mediation of tissue eosinophilia in hypersensitivity reactions. II. Separation of a delayed eosinophil chemotactic factor from macrophage chemotactic factors.

In anaphylactic cutaneous lesions induced by DNP-ascaris extract in the guinea-pig, the time-course of delayed tissue eosinophilia was found to parallel that of the macrophage reaction, reaching its peak in 24 h. Macrophages could be differentiated from lymphocytes by the numerous lysosomal granules which stained for acid phosphatase. Extracts from such skin lesions contained a delayed eosinophil chemotactic factor and two different macrophage chemotactic factors. Most of the delayed eosinophil chemotactic factor was separated from the two macrophage chemotactic factors by gel filtration on Sephadex G-100 and Sephadex G-200 in that order. The eosinophil chemotactic factor after re-chromatography on Sephadex G-I99 showed no or little chemotactic activity for macrophages.

Anaphylaxis↗
PubMedDate not supplied

Hematopoietic tissues, as a playground of receptor tyrosine kinases of the PDGF-receptor family.

Three receptor tyrosine kinases of the PDGF receptor family (RTKP) that clustered within 1000 Kb of the mouse chromosome 5 constitute an interesting unit that are expressed in three distinct cell lineages essential for constructing hematopoietic tissues. Namely, the c-kit gene that is expressed in hematopoietic stem cells is flanked by pdgfr alpha and flk genes expressed respectively in stromal cells and vascular endothelial cells. In this article, we review our results on their expression in the embryonic hematopoietic tissues. We found that co-expression of Flkl and c-Kit was frequently detected either in vascular endothelial cells or hematopoietic cells in the early hematopoietic tissues. On the other hand, the three RTKPs are expressed in different cell lineages in the fetal liver. On the basis of this finding, we propose two modes of embryonic hematopoiesis; hematogenic angiopoiesis and hematopoiesis.

Animals↗
PubMedDate not supplied

The effect of methotrexate (MTX) on expression of signalling lymphocytic activation molecule (SLAM) in patients with rheumatoid arthritis (RA) and its role in the regulation of cytokine production.

OBJECTIVE: To investigate the effect of methotrexate (MTX) on cytokine production by activated CD4+ T-cells in patients with rheumatoid arthritis (RA). METHODS: The effect of MTX on intracellular expression of interferon-gamma (IFN-gamma) and interleukin-4 (IL-4), and cell surface expression of signalling lymphocytic activation molecule (SLAM) from freshly isolated peripheral blood mononuclear cells (PBMCs), and after in vitro culture with or without MTX, was analysed with flow cytometry in 18 patients with RA and 20 healthy controls. RESULTS: Intracellular expression of IFN-gamma and IL-4 on freshly isolated CD4+ T-cells was significantly higher in patients with RA than in the controls (p<0.05). Intracellular expression of both IFN-gamma and IL-4 after culture with MTX was significantly lower than those after culture without MTX in patients with RA. Although no significant difference was observed in SLAM expression on freshly isolated CD4+ T-cells between patients with RA and the controls, MTX significantly decreased SLAM expression on both activated IFN-gamma+ and IL-4+CD4+ T-cells in patients with RA. CONCLUSION: In vitro modulation of the cytokine network by MTX, IFN-gamma, and IL-4 is one of the major targets for MTX, and production of IFN-gamma and IL-4 by PBMCs may be suppressed by SLAM on activated CD4+ T-cell in patients with RA.

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