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M Kyogoku

Publications and source records attributed to M Kyogoku.

At least 55 records · Page 3Linked to original sources
PubMed1990

Recognition of N-glycosidic carbohydrates on esophageal carcinoma cells by macrophage cell line THP-1.

Cell-to-cell contact between macrophages and tumor cells is an important initial reaction in a host defense mechanism against tumor cells. The authors have studied cell surface components of human esophageal carcinoma cells recognized by macrophages. Superoxide release from THP-1 cells, a human macrophage cell line, was analyzed in their interaction with a battery of human squamous cell carcinoma cell lines (TE) originated from esophageal cancer patients. The macrophage-triggering ability of TE 1 cell line, a high stimulant, was reduced after treatment with trypsin or tunicamycin, an inhibitor of N-glycosidic glycosylation. Addition of monosaccharides was efficient in competitive inhibition of these cellular interaction. Moreover, con-A-resistant mutation of TE 1 cells was found to reduce their macrophage-triggering ability, associated with increase of L-PHA-binding capacity, suggesting substitution to the GlcNAc beta(1----6)-linked lactosamine antenna in N-glycosidic carbohydrates. These findings suggest that terminal residues of N-glycosidic carbohydrates on some esophageal carcinoma cells may contribute to the recognition sites of macrophages.

Carcinoma, Squamous Cell↗
PubMed1990

Increase of beta 1-6-branched oligosaccharides in human esophageal carcinomas invasive against surrounding tissue in vivo and in vitro.

The -GlcNAc beta 1-6Man- (beta 1-6) branched N-glycosidic oligosaccharides expressed on tumor cells have been found to contribute to malignant and metastatic potential in experimental tumor models. Phaseolus vulgaris leukoagglutinin (L-PHA) requires the beta 1-6-linked lactosamine antenna for high-affinity binding and was used histochemically to characterize the distribution of these sugar structures in human esophageal squamous cell carcinomas from 42 patients. Leukoagglutinin-reactive carcinoma cells in the invasive tumors were distributed predominantly on the outer surface of the tumor adjacent to the surrounding tissue. Furthermore, when TE 1 cells, a human esophageal squamous cell carcinoma line, were cultured in a collagen gel matrix to obtain colonies in a three-dimensional form, these colonies exhibited high affinity for L-PHA binding only in the outer cell layer facing the collagen matrix, unrelated to the cell growth cycle. These findings suggest that the increase in beta 1-6-branched oligosaccharides in esophageal carcinomas is an important trait of the tumor in the invasion into the surrounding tissue.

Acetylglucosamine↗
PubMed1990

[Qualitative and quantitative studies of synovial lesions in early rheumatoid arthritis demonstrated by immunocytochemistry with monoclonal antibodies].

We investigate the early stage of synovial lesions in 12 cases of rheumatoid arthritis (RA), which were diagnosed according to the criteria refined by America Rheumatism Association in 1987. The purpose of this study was to follow the inflammatory process from beginning to well known typical inflammatory features which are composed of a lot of lymphocytes and proliferated capillaries and the synovial cells. The characteristics of this study were that 1) the arthroscopy was applied for observation and getting synovial tissues, 2) 7 kinds of monoclonal antibodies were used for biopsied synovial tissues in immunohistochemistry study, further 3) qualitative and quantitative methods were adopted for identifying the infiltrating cells. These methods have developed recently in the fields of orthopaedics and immuno-histopathology, respectively. In very early stage, first, HLA/DR positive cells with large elongated cytoplasm accompanied but a few processes were found in pericapillary regions. These were neither macrophages nor lymphocytes. Following them T lymphocytes appeared and B lymphocytes appeared to aggregate in later. Quantitatively the number of HLA/DR positive cells including macrophages, B lymphocytes and a part of T lymphocytes and of Interstitial cells, increase and occupied the fairly large number of ratio in the cells of synovial tissues in RA.

Adult↗
PubMed1989

[Proposal of revised criteria for malignant rheumatoid arthritis].

The diagnostic criteria for malignant rheumatoid arthritis (MRA), which was proposed by the Research Group of MRA and periarteritis nodosa supported from the Ministry of Health and Welfare has been widely used since 1973. This diagnostic criteria was established for selecting RA patients with life-threatening extraarticular manifestations caused by vasculitis. However, in practice, RA patients with extraarticular involvements related to vasculitis, as well as, cases which were not related to vasculitis were diagnosed as MRA in this criteria. Because of the aforementioned and after research, we revised the diagnostic criteria for MRA. At first, we defined MRA as RA patients having intractable and severe extraarticular manifestations by various causes including vasculitis. One hundred and sixty-nine patients with MRA and 227 patients with RA from 39 medical facilities were analysed. Sixteen extraarticular clinical manifestations and 9 laboratory findings were compared between MRA and RA patients. Comparison of specificity in each criterion for MRA was made by using the Second quantitative analysis. Thereafter, the combinations of the variables which were most specific to MRA were studied. At the same time, sensitivity and specificity for MRA were also studied. The revised criteria are as follows: A. Clinical and Laboratory Findings--(1) visceral infarction, (2) myocarditis, (3) skin ulcer or skin infarction, (4) episcleritis or iritis, (5) polyneuritis, (6) high titers of rheumatoid factor, (7) immune complexes or low complement levels, (8) subcutaneous nodule, (9) pleuritis or pericarditis, (10) interstitial pneumonitis or lung fibrosis. B. Histopathological Findings from Biopsy Specimens--necrotizing vasculitis and/or granulomatous vasculitis and/or endoarteritis obliterans in small and/or medium size arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Arthritis, Rheumatoid↗
PubMed1989

Analysis of granulomatous arteritis in MRL/Mp autoimmune disease mice bearing lymphoproliferative genes. The use of mouse genetics to dissociate the development of arteritis and glomerulonephritis.

MRL/Mp mice bearing the lymphoproliferation gene (lpr) spontaneously develop systemic granulomatous arteritis coincident with glomerulonephritis (GNP). Although the association of lpr-dependent lymphoproliferation in these mice seems to be a prerequisite for the development of granulomatous arteritis, the genetic basis is poorly understood. The first approach to this problem was to study the ability of another, nonallelic, lymphoproliferative gene, gld (generalized lymphoproliferative disease), inducing arteritis in MRL/Mp mice. The gld gene was placed on an MRL/Mp background by producing reciprocal (MRL/Mp-+/+ X C3H/Hej-gld/gld)F2 hybrid mice. Seventeen percent of these mice with lymphoproliferation had arteritis and GNP, suggesting that more than one lymphoproliferative gene could induce GNP and arteritis in an MRL/Mp background. Next, the effect of rearrangements in the genetic background of MRL/Mp-lpr/lpr mice by hybridization with non-autoimmune lpr-bearing mice was examined. This was done by making MRL/Mp-lpr/lpr X reciprocal (MRL/Mp-lpr/lpr X C57BL/6-lpr/lpr)F1 mice. Thirty-three percent of these mice developed arteritis, but one third of these did not get GNP, thus showing that susceptibility to arteritis was separate from GNP. The histopathologic features of the arteritis in both the F2 hybrids and the backcross mice were granulomatous and were identical to those seen in MRL/Mp-lpr/lpr mice. These findings suggested that it might be possible to dissociated two components (arteritis and GNP) of a severe autoimmune disease of MRL/Mp mice and to study their pathogenesis separately.

Animals↗
PubMed1988

Mutant monoclonal antibodies with select alteration in complement activation ability. Impact on immune complex functions in vivo.

Mutagenesis of mAb is a useful means for studying the biologic and pathologic functions of immune complexes. Treatment of the Hy-1.2 hybridoma-producing IgG2a-anti-TNP antibodies with ethylmethanesulfonate provided us with a mutant clone, producing antibodies with reduced capacity for C activation. The antibodies retained normal Ag-binding capacity, staphylococcal protein A reactivity, and association to FcR for IgG on murine macrophages. No significant polypeptide deletion or class-switch was observed, but a significant change in clonotype was revealed by IEF. Intravenous injection of the mutant antibodies in immune complex form induced different tissue distributions of Ag in mice; i.e., more in kidneys and less in spleen, and developed more mesangial deposits in renal glomeruli compared with those of the wild type. Moreover, the production of granulomatous lesions in vivo caused by immune complexes of TNP-Sepharose was augmented by using mutant antibodies. These lesions demonstrated an enhanced accumulation of macrophages with multinucleated giant cells. Availability of this kind of mutant mAb is thus helpful in the elucidation of the biologic functions and consequences of immune complexes.

Animals↗
PubMed1988

A new decalcifying technique for immunohistochemical studies of calcified tissue, especially applicable to cell surface marker demonstration.

We have developed a new decalcifying technique for use in light and electron microscopy studies utilizing immunohistochemical staining of calcified tissues. Specimens containing calcified tissues can be adequately decalcified at a pH of 7.1-7.4 and temperature of -5 degrees C, without freezing, by use of a solution containing EDTA, sodium hydroxide, and glycerol. In this study, Leu-2a, Leu-3a, Leu-4, Leu-7, Leu-12, Leu-14, Leu-M1, Leu-M2, Leu-M3, and HLA-DR-positive cells in destructive lesions of bone tissues from patients with rheumatoid arthritis and osteomyelitis were successfully detected immunohistochemically. Furthermore, the presence of HLA-DR antigen on the surface of the infiltrating cells in the same lesions could be demonstrated using the immunoelectron microscopic technique. The results reported here have not previously been obtainable using conventional decalcifying techniques.

Antibodies, Monoclonal↗
PubMed1987

Pathogenesis of arteritis of SL/Ni mice. Possible lytic effect of anti-gp70 antibodies on vascular smooth muscle cells.

The SL/Ni strain of mice spontaneously develops a necrotizing polyarteritis (NPA) that is histologically quite similar to human polyarteritis nodosa. This NPA most frequently affected parametrial tissues and/or ovaries of females and small arterioles of the major salivary glands. Electron microscopic studies of early arterial lesions revealed massive budding of C-type particles from arterial smooth muscle cells just before or at the onset of arteritis. In addition, binding of mouse IgG and C3 to the plasma membrane of virus-producing smooth muscle cells was shown by immunoelectron microscopy. Antibody-bound muscle cells showed disintegration of their plasma membrane, but degeneration and necrosis of muscle cells were not associated with dense infiltration of neutrophils. SL/Ni mice had natural antibodies that bound specifically to a fibroblast cell line infected with an endogenous ecotropic murine leukemia virus (MuLV) recovered from a SL/Ni mouse. Most of the natural antibodies were cytotoxic in the presence of murine complement. Western blot immunoassays revealed that among 14 SL/Ni female mice tested, all of the 9 mice that were affected by arteritis had anti-gp70 antibodies, while the 3 anti-gp70- mice were not affected. The presence of anti-p30 or anti-p15 (anti-p12) antibodies, which were also detected in some SL/Ni mice, did not correlate with the development of arteritis. These results strongly support the hypothesis that NPA in SL/Ni mice is mediated by the lysis of arterial smooth muscle cells due to the deposition of cytotoxic natural antibodies directed to cell membrane-bound gp70 molecules of an endogenous ecotropic MuLV.

Animals↗
PubMed1987

Immunohistochemical localization of fibronectin in the human placentas at their different stages of maturation.

The distribution of fibronectin in the human placenta was studied by the aid of the immunoperoxidase technique using specific antibodies against it. In the early chorionic tissue, fibronectin was distributed along the trophoblastic basement membrane, on the wall of fetal blood vessels, in the connective tissue core, and in the cytotrophoblastic cell columns. In the term placenta, this glycoprotein was detected mainly on the fetal blood vessels and less intensely in the stroma, but not along the trophoblastic basement membrane. Endothelial cells of the blood vessels, fibroblastic cells in the stroma, and unidentified cells in the cytotrophoblastic cell columns were immunostained positively for fibronectin. These data suggest that fibronectin of the placenta is produced locally and retained in the tissue, if not all.

Antigens↗
PubMed1987

A pathological analysis of Kawasaki disease--with some suggestions of its etio-pathogenesis.

As a conclusion, reviewing the pathological findings of KD and several animal models it will be clear that: 1) Kawasaki Disease is a systemic disease that attacks infants of immature immunological and angio-structural background. 2) The nature of the disease is that of "one-hit" type which attacks infants with some deranged biological conditions. The fate and grade of the disease depend merely on the grade of the hit in the first week of illness. The following is just a course of adaptation and repair of the injured sites. 3) The disease starts from the initial seroexudative inflammation, and through its transient granulocyte-leading stage, comes to the final (lymph) mono-histiocyte dominant interstitial inflammation, which seems to concentrate to the arterial wall. 4) The grade of granulocyte infiltration, the high potentiality of the mesenchymal cells and the growth factor derived from aggregated platelets and destroyed muscle cells seem to decide the fate of arterial lesion. 5) This is a disease which is different from a usual infection, or immune-complex induced disease. But from a pathological point of view, it "could" be caused by some "toxic substance including some virus," proliferated in the blood stream or endothelium of the infants with somewhat deranged defense mechanisms. 6) The information from two strains of mice, SL/Ni and MRL/Mp-lpr/lpr, which develop arteritis with a participation of retrovirus, will be useful to evaluate the retrovirus theory of KD.

Animals↗
PubMed1987

Immunopathology of murine lupus-overview, SL/Ni and MRL/Mp-lpr/lpr-.

Murine lupus is a useful animal model for the study of disease based on some defect in the immune system including the so-called collagen diseases. Seven strains are available in Japan; NZB, NZB/WF1, MRL/Mp-lpr/lpr, BxSB, SL/Ni, NC and C3H/HeJ-gld/gld. Characteristics of these strains of mice are outlined. Care should be taken about applying the knowledge or information obtained from animal models to the analysis of related human disease because there are various genetic or species barriers which cannot be overcome. Therefore, it is rather dangerous to conclude that the pathogenesis of some human disease is similar to that of an animal model from a study of the latter. Therefore, one should divide the data obtained from animal experiments into "factors" and insert each factor in the "formula" of a human disease in order to better understand it. Recent studies by the authors on two strains of lupus mouse; SL/Ni and MRL/Mp-lpr/lpr from such a standpoint are presented and discussed in detail.

Animals↗
PubMed1986

Tumor-associated glycoprotein (TAG-72) detected in adenocarcinomas and benign lesions of the stomach.

Murine monoclonal antibody (MAb) B72.3, prepared against a membrane-enriched extract of metastatic carcinoma and reactive with a high-molecular-weight determinant, designated tumor-associated glycoprotein (TAG)-72, was shown to be reactive immunohistochemically with 97% of a variety of primary adenocarcinomas of the stomach (n = 40). All "early" gastric carcinomas were reactive with MAb B72.3, although the average percentage cellular reactivity was lower than in "advanced" carcinomas. TAG-72 antigen was detected in benign lesions (i.e. adenomatous polyps and hyperplastic polyps) with intestinal metaplasia. Dysplastic lesions characterized by cellular atypia, abnormal differentiation, and disorganized mucosal architecture demonstrated higher TAG-72 expression than non-dysplastic epithelia. In contrast, normal gastric mucosa was generally non-reactive with MAb B72.3. Assays using serial sections of normal, benign and malignant gastric tissues with two MAbs (B1.1 and COL-6) directed against distinct epitopes of carcinoembryonic antigen (CEA) demonstrated differential reactivity, confirming that TAG-72 and CEA are distinct, non-coordinately expressed antigens. Our results suggest that TAG-72 antigen may be expressed in malignant and dysplastic epithelial cells, as well as in intestinalized epithelium of the stomach which has been closely related to subsequent carcinoma development. Hence, MAb B72.3 may be a useful immunohistochemical adjunct for detecting early foci of adenocarcinomas and premalignant lesions of the stomach.

Adenocarcinoma↗