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  • Title: The immunological competence of subjects with sarcoidosis.
    Author: Mangi RJ, Dwyer JM, Gee B, Kantor FS.
    Journal: Clin Exp Immunol; 1974 Dec; 18(4):505-17. PubMed ID: 4283120.
    Abstract:
    Immunological competence in sarcoidosis was measured by in vivo and in vitro immunological testing of eighteen subjects who had never been treated with prednisone, and eleven subjects treated with prednisone. Three of the latter group had been studied before steroid therapy. Cutaneous delayed hypersensitivity was assessed by intradermal skin testing with five antigens. Thymus-derived `T' lymphocytes and bone marrow-derived `B' lymphocytes were enumerated and the ability of lymphocytes to respond to stimulation with phytohaemagglutinin (PHA), Candida albicans and allogeneic irradiated lymphocytes (mixed lymphocyte reaction) was measured and compared to results obtained with lymphocytes from healthy subjects. The non-steroid-treated and the steroid-treated groups did not respond as well as a control group to intradermal challenge. The responses of lymphocytes from patients with untreated sarcoidosis to PHA and Candida albicans was normal but the response to allogeneic lymphocytes was reduced. In comparison stimulation indices for lymphocytes from the group who were receiving steroids were significantly reduced, with eight of eleven individuals having abnormal responses. Significant reduction in T lymphocytes was observed in only three of eleven of the non-steroid-treated subjects and five of ten of the steroid-treated subjects that were studied. Studies on patients before and after steroid therapy suggest that steroid therapy and not sarcoidosis was responsible for the poorer responses of the steroid-treated group. The most striking finding of this study was the marked disparity between the cutaneous reactivity to Candida albicans, which was abnormal, and the in vitro lymphocyte response to this antigen which was normal. This suggests that the anergy of sarcoidosis cannot be attributed to an inherent lymphocyte dysfunction or to a depletion of these cells.
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