Japanese Journal of Clinical Immunology
Online ISSN : 1349-7413
Print ISSN : 0911-4300
ISSN-L : 0911-4300
Volume 13, Issue 4
Displaying 1-11 of 11 articles from this issue
  • [in Japanese]
    1990Volume 13Issue 4 Pages 307-319
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
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  • Yasuhiro Mizoguchi, Tohkan Shin, Norifumi Kawada, Kenzo Kobayashi, Sei ...
    1990Volume 13Issue 4 Pages 320-327
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    When trinitrophenylated hepatocytes were intravenously injected into trinitrophenylated liver protein-sensitized guinea pigs through mesenteric vein, hepatic cell necrosis was seen to a large extent in all of the guinea pigs and the values of serum GOT and GPT increased to 1, 067±265 and 101±24U/l 24 hours later. However, when trinitrophenylated hepatocytes were injected into trinitrophenylated liver protein-sensitized guinea pigs which had been administered with Sho-saiko-to 30, 24 and 6 hours before, only spotty necrosis could be seen and massive hepatic cell necrosis was not seen in any of the guinea pig. In addition, the values of GOT and GPT remarkably improved.
    These results suggested that Sho-saiko-to is effective for the immunologically-induced allergic hepatic cell injury model.
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  • Mikiro Iseki, Yukihiko Koizumi, Mitsuru Osano
    1990Volume 13Issue 4 Pages 328-336
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Serum concentrations of IgG1, G2, G3, and G4 were determined in 394 healthy Japanese (cord blood, newborns, and 0-35 years, males 228, females 166) by means of single radial immunodiffusion and ELISA. The mean concentrations and ranges (two standard deviations) were as follows: cord blood, n=30, IgG1 853 (543-1, 340)mg/dl, G2 438 (210-648)mg/dl, G3 20 (2-217)mg/dl, G4 24 (2-304)mg/dl, 1 year, n=33, IgG1 733 (311-1, 726)mg/dl, G2 161 (-343)mg/dl, G3 27 (3-204)mg/dl, G4 4 (0.4-50)mg/dl, 6-8 years, n=30, IgG1 841 (473-1, 496)mg/dl, G2 344 (68-620)mg/dl, G3 26 (4-151)mg/dl, G4 17 (3-109)mg/dl, adults, n=90, IgG1 791 (402-1, 556)mg/dl, G2 621 (281-961)mg/dl, G3 28 (3-258)mg/dl, G4 34 (7-161)mg/dl.
    Some healthy subjects have IgG subclass levels which fullfill the tentative criteria for IgG subclass deficiency proposed by the working group of Japanese Ministry of Health, and these deta indicated that there is a significant overlap in serum IgG subclass levels between healthy subjects and the criteria. It could be suggested that IgG subclass deficiency should not be diagnosed based solely on the laboratory data.
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  • with special reference to IL-2 receptor and ornithine decarboxylase activity on CD8+ cells
    Izumi Kishi
    1990Volume 13Issue 4 Pages 337-345
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Much importance has been attached to immune abnormalities in the pathogenesis of Behçet's disease. This study was conducted to examine whether any of antigens (retinal santigen and/or cell wall antigen from streptococcus pyogenes) acts stimulatory in Behçet patients for the expression of IL-2 receptor (IL-2R) on the peripheral T cells and the production of soluble IL-2R. Ornithine decarboxylase (ODC) activity was also determined. The corresponding responses were much lower and often negligible, whereas their responses to PHA were consistently higher than those of the antigens. The results indicate that these antigens do not share common T cell-recognized epitopes. On the other hand, remarkable enhancement of ODC activity was demonstrated by PHA stimulation, combined with the evidence of increased induction of cell group with CD8+Leu15-. Cyclosporin A showed profound suppression of ODC activity on T cells from the patients, suggesting that ODC-suppressing may play an important role in the treatment of Behçet's disease in consequence of inhibitory effect against induction of allo-reactive cytotoxic T cells.
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  • Tomoomi Nagakane, Toshio Ogura, Koji Nishiya, Masamitsu Natsumeda, Tos ...
    1990Volume 13Issue 4 Pages 346-355
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Bucillamine is a compound of tiopronin which has anti-rheumatic action pharmacologically based on the similar chemical structure of D-penicillamine. We studied the clinical profile and the precise histological and immunological changes in kidney tissue in five patients with rheumatoid arthritis (RA) who had the profound proteinuria along with the bucillamine (BU) therapy. There was no specific predisposition for BU-induced proteinuria in clinical profiles of five RA patients as age, disease duration, disease activity and co-given drugs except that all of patients were female. Urinalysis revealed proteinuria in all 5 patients (2 patients: nephrotic syndrome) and microscopic hematuria in 4 out of 5 of patients. Renal failure was not observed in all patients. The renal biopsy was performed in 4 patients. The histological findings by light microscopy, fluorescent antibody technique and electron microscopy demonstrated membranous glomerulonephritis (MGN), i.e. positive staining of _??_gG and electron dense subepithelial deposits in glomerular basement membrane (GBM). Nevertheless, the number of subepithelial deposits in GBM was smaller and the location was scattered compared with idiopathic MGN. The total dosis of BU administration in these patients varied from 7.9g to 128g (average: 41.6g). The causes of BU-induced nephropathy were not known. DLST by BU was, however, positive in 2 out of 5 patients. The outcome of BU-induced proteinuria seemed to be good since one of the patients had the renal failure and the amount of proteinuria was decreased or disappeared by steroid therapy or discontinuation of BU. Thus, the abnormal responses of cellular immunity to this drug might involve in the development of BU-nephropathy.
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  • Kunio Yanagida, Shuhei Takemura, Wataru Fukuda, Masayuki Okamoto, Taka ...
    1990Volume 13Issue 4 Pages 356-364
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Complement fragments, C4d, iC3b and Bb are generated through activation of the complement pathway. The plasma levels of the fragments were measured by means of enzymeimmunoassay to study the clinical significance of them in some connective tissue diseases.
    The plasma levels of C4d and iC3b were significantly elevated in patients with SLE, MCTD and RA. The levels of Bb was significantly elevated in plasma from SLE and RA. In SLE, total complement hemolytic activity, CH50, and these fragments levels did not correlate. It is supposed that there are many factors which influence the complement activity in patients with hypocomplementemia, such as the existence of inhibitors or inactivators, reduced synthetic rates and increased rates. The measurement of complement fragments in serial plasma samples obtained from patients with connective tissue diseases, especially with SLE, seemed to be simple and useful to evaluate the activation of complement in vivo.
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  • Takashi Takizawa, Masanori Yamamoto, Susumu Nishinarita, Shigemasa Saw ...
    1990Volume 13Issue 4 Pages 365-372
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Fibronectin (FN) levels in plasma of patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), scleroderma, dermato-/polymyositis (DM/PM) and mixed connective tissue disease (MCTD), and FN levels in synovial fluid of patients with RA and osteoarthritis (OA) were measured by radioimmuno-inhibition assay. The mean FN level in plasma of SLE patients was higher than that of normal controls (603±104μg/ml vs 339±28μg/ml, p<0.01). In active SLE group, the mean FN level was higher than that of inactive group (764±135μg/ml vs 377±82μg/ml, p<0.01). The mean FN level in plasma of RA patients (469±43μg/ml) was higher than that of normal controls (p<0.01). In RA, plasma FN level did not correlate with the clinical activity. The mean FN level in synovial fluid of RA patients (1, 148±224μg/ml) was higher than that of osteoarthritis patients (548±60μg/ml, p<0.01) and that of plasma of RA patients (p<0.01). In RA, a significant correlation between the FN level in plasma and that in synovial fluid was observed. The mean FN level in plasma from patients with PSS (483±92μg/ml) and MCTD (1, 240±480μg/ml) were higher than that of normal controls, but the FN of DM patients was in the normal range (293±72μg/ml). These results suggest the quantitation of FN in plasma and synovial fluid is useful for the evaluation of the pathophysiology of collagen diseases.
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  • Lymphocyte subsets, blastogenesis and NK activity of peripheral lymphocytes, and serum IFN activity
    Kazunori Yoneda, Tetsuya Yamamoto, Tokio Osaki
    1990Volume 13Issue 4 Pages 373-383
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Immunological parameters such as lymphocyte subsets, blastogenesis, natural killer (NK) activity of peripheral blood lymphocytes, and serum interferon activity were investigated on 40 oral cancer patients composed of 20 good prognosis cases without metastasis (good group) and 20 bad prognosis/metastasis-positive cases (bad group). The results obtained were as follows.
    1) While each lymphocyte subset proportion in good group was not significantly different from that in healthy controls, Leu3a+8+ cell proportion in bad group was significantly lower (p<0.05) than the controls', and statistically significant decreasing (p<0.001) of Leu3a+8+ cells with chemo/radiotherapy was observed in good group.
    2) Lymphocyte blastogenesis was correlated with Leu3a+8+ cell proportion (p<0.001), and blastogenic response in bad group was inferior to the controls' lymphocyte response.
    3) No significantly different NK activity could be observed among two patient groups and healthy controls, but serum IFN activity in good group was significantly higher than that in controls (p<0.01).
    From the above, it was revealed that immune condition relates with the clinical feature of oral cancer patients, and Leu3a+8+ cell proportion appears especially useful for the evaluation of the patient's status.
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  • Mitsuo Ohkubo, Syunji Kaise, Tomoe Nishimaki, Takao Moritou, Reiji Kas ...
    1990Volume 13Issue 4 Pages 384-390
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    A 53-year-old woman has been troubled with oral aphtha and genital ulcer since 1977. Her physical and laboratory findings were consistent with a diagnosis of incomplete Behçet's disease. In 1980 she noticed multiple purpura in her extrem ities with pain. The purpura has been appeared periodicaly in her lower extremities. In 1987 the purpura extended to her upper extremities.
    Her laboratory findings on admission were summarized as follows: Erythrocyte and thrombocyte count, bleeding time and coagulation time were normal. Autoantibodies against erythrocytes, thrombocytes, cardiolipin, DNA and IgG (rheumatoid factor) were not noted. But Rumpel-Leede test and skin test by injection of her own erythrocyte were positive. Especially by injection of lysed erythrocyte, the redness was marked.
    A diagnosis of autoerythrocyte sensitization syndrome; Gardner & Diamond disease; (AES) was considered on her symptoms.
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  • Kozo Onami, Yutaka Kikuta, Akiko Yoshida, Yae Nakagawa, Katsuaki Ukai, ...
    1990Volume 13Issue 4 Pages 391-400
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    A case of primary biliary cirrhosis associated with Sjögren's syndrome, CRST syndrome and eary gastric cancer was reported. A 73-year-old female has been suffered from Raynaud's phenomenon, sclerodactyly, arthralgia and Sicca syndrome. She was diagnosed as Sjögren syndrome and CRST syndrome with her additional symptoms of calcinosis and telangiectasia. The specimen of liver taken of the occasion of gastrectomy of her stomach for early gastric cancer (Type IIc, moderately differrentiated adenocarcinoma) showed a histology of primary biliary cirrhosis showing chronic non supprative destructive cholangitis with mononuclear cell infiltration in Glisson's sheath followed by granuloma. The titers of anti-mitochondria, anti-DNA antibody and eosinophilia decreased during the period of observation. However, the intensity of PPD reaction and PHA stimulation test was unchanged. Her HLA showed DR 4 and DR 9. It was suggested that CRST syndrome, PBC and eary gastric cancer might related to the immunological abnormality in broad spectrum observed in Sjögren's syndrome.
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  • suspected maturational defect from CD4+CD45R+ to CD4+CD45R- phenotype
    Masayuki Nagasawa, Junichi Yata
    1990Volume 13Issue 4 Pages 401-410
    Published: August 31, 1990
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    The author reported a case of 18-month-old girl with hypogammaglobulinemia. She had recurrent upper respiratory tract infections since 6 month old. Serum immunoglobulin values were IgG 311 mg/dl, IgM 15 mg/dl and IgA 45 mg/dl respectively. Antibodies against varicella and polio were negative despite vaccination, but IgM antibody against pertussis was positive after vaccination. Immunophenotypical analysis of PBL revealed normal numbers of CD20+, CD8+, CD4+ and CD16+ cells, but increased ratio of CD4+CD45R+/ CD4+ cells. In vitro, B cells proliferated well in response to SAC, T-cell independent B cell mitogen, and differentiated to secrete enough amount of IgG, IgM and IgA in combination of SAC and IL2, indicating that B sells were maturated enough to respond to cytokines with BCDF activity and secrete Ig. In PWM-driven Ig synthesis, patient PBL secreted low to moderate amount of IgM and very low amount of IgG and IgA. In co-culture assay, patient T-cells did not help control nT to secrete Ig, but control T partially helped patient nT to secrete Ig. Proliferative response of patient T to PHA was decreased and recovered by exogeneous IL2 completely, indicating impaired production of IL2. In vitro change of CD45R expression on CD4+ T-cells in response to PHA plus IL2 was also impaired compared to control. These results may suggest that there is a maturational defect or delay in patient's T-cells from CD4+CD45R+ to CD4+ CD45R- phenotype, and this defect could be responsible for patient T-cell's disability to help Ig production. This impaired T-cell function might be transient or not is remained elucidated, but this case is unique, and helpful for understanding of mechanism of hypogammaglobulinemia which might be due to T-cell dysfunction.
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