Japanese Journal of Clinical Immunology
Online ISSN : 1349-7413
Print ISSN : 0911-4300
ISSN-L : 0911-4300
Volume 7, Issue 4
Displaying 1-11 of 11 articles from this issue
  • Hiroko Tsutsui, Yasuhiro Mizoguchi, Hiroko Katoh, Keiji Miyajima, Taka ...
    1984 Volume 7 Issue 4 Pages 197-201
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Peritoneal macrophages become cytotoxic for the tumor cells by stimulating with lipopolysaccharide prepared from a Gram-negative bacteria. Although these cytotoxic action on tumor cells was not demonstrable when macrophages were treated with lower dosis of LPS than 1μg/ml, simultaneous addition of methyl-vitamin B12 with LPS resulted in a significant augmentation of tumor cell cytotoxicity. Since vitamin B12 alone did not induce any cytotoxic macrophages, vitamin B12 may increase in the actvation of macrophages partially stimulated with low dosis LPS.
    Download PDF (274K)
  • Relationship to the tachyphylaxis
    Yoshiro Tanizaki, Haruki Komagoe, Jun Ohtani, Masanori Maeda, Hikaru K ...
    1984 Volume 7 Issue 4 Pages 202-207
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
  • Jun Koide, Tohru Abe, Tsutomu Takeuchi, Osamu Hosono, Kouichi Amano, M ...
    1984 Volume 7 Issue 4 Pages 208-215
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    In the present study, we demonstrated that peripheral blood T lymphocytes from active patients with systemic lupus erythematosus (SLE) spontaneously produced B cell stimulatory factor (BSF) after 2 days' culture. The BSF contained B cell growth factor (BCGF) and B cell differentiation factor (BCDF) activities. These BCGF and BCDF activities spontaneously produced by T cells from active SLE patients were almost as potent as that of PHA-stimulated T cells from normal individuals and inactive SLE patients. Furthermore, B lymphocytes from active patients with SLE proliferated or secreted IgG antibody in response to BCGF or BCDF alone in the absence of anti-IgM or SAC-stimulation. Particulary, B cells from active SLE patients produced marked IgG in response to BCDF. The activity of BCGF or BCDF spontaneously secreted by T cells from active SLE patients correlated inversely with the magnitude of responsiveness of B cells in response to BCGF or BCDF.
    Accordingly, the mechanism for B cell activation in patients with SLE seems to be heterogeneous. Such abnormal response to BSF and/or overproduction of BSF ultimately lead to polyclonal and even autoantigen-specific B cell expansion which result in the production of autoantibodies.
    Download PDF (422K)
  • Yohachiro Ohama, Sachiko Iwamoto, Yasushi Yukiyama, Shun-ichi Hirose, ...
    1984 Volume 7 Issue 4 Pages 216-223
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    The effect of anti-DNase I antibody on an enzymatic activity of DNase I and anti-DNase I antibody in collagen diseases were studied. Rabbit anti-DNase I antibody which was raised by immunization with bovine pancreatic DNase I was shown to be a DNase I inhibitor. Sera from 75 SLE patients, 28 RA patients, 9 PSS patients and 30 healthy individuals were examined to detect antibody to DNase I by Farr test. Radioactive iodine-labeled purified bovine pancreatic DNase I was used as an antigen in the assay. Mean antibody-value of the each group of the patients was significantly higher than that of the healthy group. The incindence of the antibody, regarded as positive when the value exceeded the mean value+2SD of the healthy group, was 56% in SLE, 50% in RA, 22% in PSS and 0% in healthy individuals. Possible roles of anti-DNase I antibody in collagen diseases were discussed.
    Download PDF (1011K)
  • Yasuko Murayama, Tetsushi Sakurai, Ichiro Kono, Teizo Kabashima, Kazuh ...
    1984 Volume 7 Issue 4 Pages 224-227
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    A 32-year-old-female with systemic lupus erythematosus (SLE) suddenly manifested signs of diabetes insipidus shortly after she had been placed on a high-dose prednisolone for high fever, hemorrhagic tendency, mental confusion and motor neuron abnormalities. Psychogenic polydipsia was excluded on the basis of progressive polyuria in the presence of dehydration. Tobramycin-induced tubular dysfunction was denied because of the extreme severity of polyuria, negative urinary findings and a negative rechallenge study.
    Diabetes insipidus is a rare manifestation of SLE. Vasculitis of small arteries may have been responsible for reversible ischemic changes in the hypothalamus-pituitary axis in this case.
    Download PDF (208K)
  • Hiroshi Ushijima, Kazuya Yoshino, Ryochi Fujii
    1984 Volume 7 Issue 4 Pages 228-233
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    We have experienced a female case of systemic lupus erythematosus with recurrent erythr thrombocytopenia induced by autoimmunity (Evans syndrome) and bone marrow suppression respectively in the course of the disease.
    She showed Evans syndrome and incomplete diagnostic criteria of SLE on the first admission at 10years old, Evans syndrome induced by rubella infection on the second admission at 11years old, complete diagnostic criteria of SLE on the third admission at 12years old without Evans syndrome, and erythrothrombocytopenia associated bone marrow suppression on the fourth admission at 17years old.
    “Pulse ” methyl prednisolone therapy was effective to improv the bone marrow suppresion.
    Download PDF (309K)
  • Masao Ishii, Yoshiko Matsuoka, Toshinori Ishii, Kiyoshi Takatsuki
    1984 Volume 7 Issue 4 Pages 234-239
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Complexes of lactate dehydrogenase with immunoglobulin (LDH-Ig) were detected in a case of RA. Circulating immune complex (CIC) and LDH activity were high in the serum of the patient.
    By immunofixation, binding immunoglobulins were identified with IgG (κ) and IgG (λ). IgG (λ) disappeared soon, and only IgG (κ) existed for about 4 months. The two peaks of LDH activity were shown between 4S and 7S (Peak-S), 7S and 19S (Peak-F) by gel filtration on Sephadex G-200. By solid phase anti-C3 enzymelinked immunosorbent assay (ELISA), CIC level was high in Peak-F and low in Peak-S. In the sample of Peak-F fraction, LDH activity was high in the plates coated with anti-C3, anti IgG and anti κ antibody.
    In conclusion, this is a first report that LDH-IgG binds with Complement and forms immune complexes. LDH activity was not affected by binding to IgG-C3.
    Download PDF (864K)
  • Akira Takeda, Mariko Sasaki, Nagahiro Minato, Yoshiaki Mizoguchi, Mori ...
    1984 Volume 7 Issue 4 Pages 240-246
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Although systemic lupus erythematosus (SLE) is well recognized to be associated with systemic vascular lesions, histologically proven severe vasculitis of the skin has rarely been documented in SLE literature. We had the opportunity to observe a patient with SLE who developed leukocytoclastic vasculitis in the erythematous lesion. Since this condition has received little attention, we feel that the following case report may be of interest.
    A 34-year-old woman was admitted to the hospital in July 1982 because of erythematous rashes on face, chest and both thighs.
    This patient's illness began at the age of 27 when she had fever, polyarthralgia and proteinuria. She responded well to 60mg prednisolone given at another hospital. Since then, she was maintained on varing doses of corticosteroid, and had had episodes of fever, arthralgia, facial erythema, photosensitivity and hair loss. The diagnosis of SLE was made in 1978 on her first visit at our outpatient clinic, based on clinical manifestations and a positive antinuclear antibody, LE cells and hypocomplementemia.
    She remained stable on 10mg prednisolone until July 1982 when erythematous eruptions appeared on both thighs accompanied by the flare-up of butterfly rash after going outdoors. The erythematous rashes, with burning, stinging and edema, soon spread over her thighs and anterior chest, followed by multiple shallow ulcerlations. She had no upper respiratory symptoms and received no particular medications.
    On admission, laboratory examination revealed microscopic hematuria and granular casts in urinalysis, positive CRP, hypergammaglobulinemia, an elevated anti-DNA antibody and hypocomplementemia. The circulating immune complex was elevated to 24.6μg/ml. A biopsy specimen of an erythematous lesion on a thigh showed leukocytoclastic vasculitis in the dermis containing numerous polymorphonuclear leukocytes and nuclear debris. Fibrinoid degeneration of walls of a few vessels was also found. Immunofluorescent staining demonstrated positive fluorescence for IgM, Clq, C3 and fibrinogen in the small vessel walls. She was treated with 40mg prednisolone and skin lesions gradually healed, accompanied by an improvement in laboratory findings.
    The leukocytoclastic vasculitis in this case was considered to be a manifestation of SLE, since the development of it was closely associated with exacerbation of SLE and no other apparent causes were found.
    Download PDF (2077K)
  • Taijiro Ishiyama, Naoki Sugaya, Tatsuo Miyayama, Masakuni Sugimoto, Yo ...
    1984 Volume 7 Issue 4 Pages 247-253
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    A 52 year-old female was admitted to our hospital in August 1982, for a tumor on her left palm, which revealed malignant melanoma by biopsy.
    The laboratory findings were as follows: the erythrocyte sedimentation rate (ESR) was 56mm/hr. The plasma total protein was 8.0g/dl with monoclonal IgA of 3, 496mg/dl. Bence-Jones protein in the urine and punched out lesions in X-ray film were negative. The bone marrow smear showed 11.7% of atypical plasma cells. A diagnosis of multiple myeloma (IgA, K type) was done.
    The tumor was resected and treated by DTIC for 5 days. And plasma IgA was reduced to 2, 438mg/dl by the treatment with prednisolone (30mg/dl), cyclophosphamide (50mg/dl) and vincristine (1mg/week).
    Her 2nd admission to our hospital was in August 1983 with the complaint of the lymph node swelling was which was a metastasis of malignant melanoma at her left axilla. Physical examination disclosed marked hepatomegaly with hepatic dysfunction. Her clinical condition was not improved by OK-432 and prednisolone therapy.
    The autopsy showed multiple metastasis of malignant melanoma to the various organs and also metastasis to the bone marrows.
    Download PDF (2159K)
  • Masayuki Tsujisaki, Kohzoh Imai, Mitsuo Suga, Tetsuo Ohshima, Yumiko I ...
    1984 Volume 7 Issue 4 Pages 254-260
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    A 23 year-old male who had a past history of recurrent infection, was admitted to our hospital with the complaint of general malaise and fever. Laboratory examination revealed IgG 430mg/dl, IgA 62ml/dl and IgM 43mg/dl with hypertransaminasenemia, in conjunction with HBs-Ag (+) and HBe-Ag (+). Liver biopsy specimen showed a lobular massive necrosis with proliferation of the small biliary ducts and with slight lymphocytosis and plasmacytosis.
    Immunological examination with peripheral lymphocytes revealed the decrease of the immunoglobulin-secreting cells detected by plaque-forming-cell assay and marked reduction of OKT 4 (+) cells and of surface immunoglobulin bearing cells. In vitro culture of the unfractionted peripheral lymphocytes from this patient in the presence of pokeweed mitogen (PWM) showed a decreased immunoglobulin production when compared with the normal control. In addition, In vitro co-culture of B cells of this patient and T cells of the control in the presence of PWM revealed the decreased production of immunoglobulin, suggesting the impared function of B cells of this patient, in addition to the reduced number of B cells. In the same type of experiments, the helper function of T cells of this patient to In vitro Immunoglobulin synthesis, was found to be impared.
    Some discussions have been made concerning the hypo γ-globulinemia in cojunction with severe liver disease and the lymphocyte dysfunction of this patient.
    Download PDF (853K)
  • Kiyotaka Kawauchi, Atuko Sagawa, Yoko Shiratori, Yoriko Suzuki, Haruo ...
    1984 Volume 7 Issue 4 Pages 261-268
    Published: August 30, 1984
    Released on J-STAGE: January 22, 2009
    JOURNAL FREE ACCESS
    Three cases of necrotizing lymphadenitis with depressed natural killer activity were reported. Necrotizing lymphadenitis, which is a benign disorder, has some characteristic manifestations such as occurrence in young people, leukopenia, elevation of serum LDH level, and so on. All of our cases presented these characteristic features. Although the etiology of necrotizing lymphadenitis is not yet known, participation of immunological mechanisms has recently been found to contribute partly to the induction of this disease. On immunological examination, depressed natural killer activity and the dissociation of natural killer activity from antibody-dependent cell-mediated cytotoxicity were observed in all our cases. In analyzing the depressed natural killer activity, plasma and serum inhibitors of the activity were not detected, and it was shown that the patient's natural killer cells had responded to interferon. Natural killer cells are important effector cells in cellular immunity and are cytotoxic to some tumor cells and virus-infected cells without antibody. The depressed natural killer activity in our cases could suggest that the disturbance of cellular immunity may have an important role on the etiology of necrotizing lymphadenitis.
    Download PDF (1456K)
feedback
Top