Japanese Journal of Allergology
Online ISSN : 1347-7935
Print ISSN : 0021-4884
ISSN-L : 0021-4884
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Volume 39, Issue 5
Displaying 1-14 of 14 articles from this issue
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  • [title in Japanese]
    Article type: Cover
    1990 Volume 39 Issue 5 Pages Cover24-
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.Cover24
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    Article type: Cover
    1990 Volume 39 Issue 5 Pages Cover25-
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.Cover25
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    [in Japanese]
    Article type: Article
    1990 Volume 39 Issue 5 Pages 437-441
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.437
    JOURNAL FREE ACCESS
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  • HYPER IgE SYNDROME-A DISEASE OF IMBALANCED ACTIVATION OF HELPER T-CELL SUBSETS?
    Shumpei Yokota, Toshihiro Mitsuda, Hiroko Shimizu, Masaaki Ibe, Zenro ...
    Article type: Article
    1990 Volume 39 Issue 5 Pages 442-451
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.442
    JOURNAL FREE ACCESS
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    Hyper-IgE' syndrome is a rare immunodeficient disorder characterized by recurrent severe staphylococcal infections of the skin and sinopulmonary tract, chronic eczematoid rashes, coarse facial features, mild eosinophilia, and markedly elevated serum IgE levels. Hyperimmunoglobulinemia D, depressed DTH, and varying degrees of decreased chemotaxis of circulating neutrophils are additional manifestations of this syndrome. The precise pathogenesis of this syndrome is unknown. The clinical manifestations and the recent research findings indicated the followings: 1)increased production of IL-4: hyperimmunoglobulinemia E, increased number of FcεR(+)-cells in peripheral blood, 2)defective production of IFN-γ: abnormal local inflammatory responses(formation of cold abscesses), chemotactic defect in the circulating neutrophils(abnormalities in IFN-γ/IL-8 pathway), depressed DTH, 3)T-cell immunodeficiency?-chronic dermatitis? 4)genetic factors(frequent familial occurrence, characteristic facial appearance with broad nasal bridge). These observations led us to postulate that both the increased production of IL-4 and the defective production of IFN-γ may be the immunopathological bases of this syndrome. Recently, these cytokines were demonstrated to be secreted by different subsets of helper T-cells, designated TH1 and TH2, in murine system, suggesting that the regulatory imbalances between IL-4 and IFN-γ in this syndrome might be due to the differential activation or inactivation of these helper T-cell subsets.
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  • HISTAMINE RELEASE FROM HUMAN LEUKOCYTES BY HUMAN RECOMBINANT INTERLEUKIN-3
    Shumsuke Kanamori, Atsuo Urisu, Kiyoshi Iimi, Yasuto Kondo, Fumiya Hor ...
    Article type: Article
    1990 Volume 39 Issue 5 Pages 452-458
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.452
    JOURNAL FREE ACCESS
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    Human recombinant interleukin-3(hrIL-3)released histamine from human leukocytes in vitro. The histamine release by hrIL-3 significantly correlated with those by anti-IgE, thrombin, and f-met. Peptide, but not by A23187. Histamine release by hrIL-3 was a Ca^<2+>-dependent reaction, as was that by anti-IgE, although the time course of histamine release by hrIL-3 was slower than that by anti-IgE. Pre-treatment of leukocytes with hrIL-3 decreased the histamine release by hrIL-3 itself, but enhanced the histamine releases by anti-IgE, f-met. Peptide, thrombin and A23187. These results suggested that the mechanism of hrIL-3-induced histamine release was different from those of anti-IgE, f-met. peptide, thrombin, and A23187. There was no significant difference between hrIL-3-induced histamine release of leukocytes from asthmatics and healthy controls.
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  • AN ANTI-HUMAN EOSINOPHIL MONOCLONAL ANTIBODY AE500 THAT REACTS ONLY WITH GRANULOCYTES FROM HYPEREOSINOPHILIC PATIENTS
    Kenichi Ochiai, Itsuo Iwamoto, Akira Kimura, Noriaki Nakagawa, Hisao T ...
    Article type: Article
    1990 Volume 39 Issue 5 Pages 459-464
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.459
    JOURNAL FREE ACCESS
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    To investigate the heterogeneity of human eosinophils, we established a murine anti-human eosinophil monoclonal antibody AE500(IgM, κ)by immunizing blood eosinophils from patients with idiopathic eosinophilia. The reactivity of AE500 with human leukocytes was analyzed by a fluorescence-activated cell sorter. AE500 reacted with all the populations of blood eosinophils and neutrophils from patients with eosinophilia(idiopathic eosinophilia, n×4 or asthma, n=), but not with those from asthmatic patients without eosinophilia(n=8)or normal subjects(n=6). AE500 did not react with granulocytes from other family members of AE500-positive individuals. These results suggest that the anti-human eosinophil antibody AE500 reacts with a cell surface antigen of blood granulocytes in a hypereosinophilic state. This anti-eosinophilic antibody would be useful in investigating the mechanism of eosinophilia in a variety of diseases.
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  • RELATIONSHIP BETWEEN BRONCHIAL HYPERSENSITIVITY AND HEREDITARY FACTORS IN RESPIRATORY TRACT ALLERGIC DISEASES BRONCHIAL ASTHMA AND NASAL ALLERGY
    Takakazu Kiya
    Article type: Article
    1990 Volume 39 Issue 5 Pages 465-475
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.465
    JOURNAL FREE ACCESS
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    Bronchial hypersensitivity was investigated by astograph in 25 nasal allergy patients without clinical symptoms of asthma and 103 healthy people from 20 asthmatic families. The data were compared with those obtained from 36 asthmatics. Intradermal skin tests and HLA typing were also performed on the members of asthmatic families. Bronchial hypersensitivity was present at a much higher rate in nasal allergy patients than in healthy people. It was also demonstrated that bronchial hypersensitivity was present even in non-asthmatics from asthmatic families, and the incidence of bronchial hypersensitivity tended to increase when complicated by nasal allergy. Increased bronchial hypersensitivity was shown in people from asthmatic families with positive skin tests to mites and house dust. Bronchial hypersensitivity seemed to be related to HLA-haplotype in the same family. The results of antigen sensitization as meassured by intradermal skin reaction test suggested that hereditary factors play some role in the development of bronchial hypersensitivity.
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  • INVESTIGATION INTO THE FREQUENCY OF CASES WITH JAPANESE CEDAR POLLINOSIS AMONG THE STUDENTS AND STAFF MEMBERS IN OUR UNIVERSITY
    Susumu Nakamura
    Article type: Article
    1990 Volume 39 Issue 5 Pages 476-482
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.476
    JOURNAL FREE ACCESS
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    Japanese cedar pollinosis, peculiar to Japan, has recently become a subject of public concern owing to the huge number of cases. Progress has been made in research on atmospheric pollen counts, consequently pollen calendars have been made and pollen forecasts are given in various parts of the country. However approach to pollinosis of this kind from physical side is not yet sufficient. In this study, the author investigated the frequency of cases with Japanese cedar pollinosis on the occasion of a periodical health examination in 892 students and 202 members of staff at our university. As a result of this study, the percentage of specific antibody carriers among the students was found to be 27.4%, and the frequency of Japanese cedar pollinosis sufferers was 12.0%, which was significantly higher than the rates found among members of staff. In addition to this, 14.7% of the students were considered to be about to become sensitized to Japanese cedar pollen, that is to say, they are"reservists"to pollinosis. Follow up investigations and preventive treatment of these cases are necessary, because they are considered very likely to become pollinosis sufferers in the future. 25.2% of the students with Japanese cedar pollinosis had asthmatic symptoms besides nasal and/or conjunctival manifestations. Accordingly it is important to examine and treat them for general allergic manifestations.
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  • INHIBITION OF ANTIGEN-INDUCED LATE ASTHMATIC RESPONSE AND BRONCHIAL HYPERRESPONSIVENESS BY CYCLOSPORIN A
    Takeshi Fukuda, Ikuo Akutsu, Toshio Numao, [in Japanese], Sohei Makino
    Article type: Article
    1990 Volume 39 Issue 5 Pages 483-487
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.483
    JOURNAL FREE ACCESS
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    We have previously demonstrated that Cyclosporin A(CyA), a T lymphocyte-selective immunosuppressive agent, reduced the delayed-phase bronchial eosinophil infiltration after antigen challenge in a guinea pig model of astham. In the present study, we studied the effects of CyA on antigen-induced late asthmatic response(LAR)and bronchial hyperresponsiveness following LAR. Guinea pigs immunized by repeated exposure to aerosolized ovalbumin(OA)were intravenously given metopirone, a cortisol synthesis inhibitor, 24 hours before and 30 minutes before antigen challenge, and to prevent death from immediate severe bronchoconstriction, chlorpheniramine maleate was also injected. After antigen challenge with high dose of OA, LAR occurred in twelve of fifteen animals(80%)and the bronchial responsiveness to acetylcholine was significantly increased. However, when guinea pigs were treated with CyA from the beginning of immunization period, the development of LAR was completely inhibited, although similar magnitude of immediate bronchoconstriction was observed, and a subsequent increase in bronchial responsiveness was partially but significantly blocked. Since CyA has been shown to suppress activation of guinea pig T lymphocytes and their production of lymphokines, these results suggest that T cell factor(s) may be important for the elicitation of LAR and the antigen-induced bronchial hyperresponsiveness.
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  • [title in Japanese]
    Article type: Appendix
    1990 Volume 39 Issue 5 Pages 488-489
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.488
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    Article type: Appendix
    1990 Volume 39 Issue 5 Pages 490-
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.490
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    Article type: Appendix
    1990 Volume 39 Issue 5 Pages 491-493
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.491
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    Article type: Bibliography
    1990 Volume 39 Issue 5 Pages 494-
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.494
    JOURNAL FREE ACCESS
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  • [title in Japanese]
    Article type: Cover
    1990 Volume 39 Issue 5 Pages Cover26-
    Published: May 30, 1990
    Released on J-STAGE: February 10, 2017
    DOIhttps://doi.org/10.15036/arerugi.39.Cover26
    JOURNAL FREE ACCESS
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