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Biomedical subjects

P Perlmann

Publications and source records attributed to P Perlmann.

At least 307 records · Page 17Linked to original sources
PubMed1970

Inhibition of cytotoxicity of lymphocytes by concanavalin A in vitro.

Human lymphocytes treated with the plant protein concanavalin A are stimulated to transform into blasts, without developing cytotoxicity for chicken erythrocytes. Prior treatment of lymphocytes with concanavalin A potentiated phytohemagglutinin-induced blast transformation and DNA synthesis but completely inhibited phytohemagglutinin-induced cytotoxicity. Inhibiton was not due to suppression of the mixed lymphocyte-erythrocyte aggregation normally caused by phytohemagglutinin. Inhibition of cytotoxicity was reversible when concanavalin A was removed from the lymphocytes by treatment with methyl-alpha-D-manno-pyranoside after 1 hour but not after 20 hours. The results indicate that blast transformation and cytotoxicity are separate expressions of lymphocyte stimulation.

Animals↗
PubMed1969

Autoantibodies to colon in germfree rats monocontaminated with Clostridium difficile.

Germfree rats monocontaminated with the anaerobic microorganisms Clostridium difficile or another Clostridium species (strain G 62) produce auto-antibodies to colon antigen. The antigen can be extracted with phenol water from the feces of germfree rats. Antibodies, demonstrable by means of passive hemagglutination of antigen sensitized sheep erythrocytes appear after monocontamination for 35 days or longer. The indirect immunofluorescence techniques, applied to sections of germfree rat colon, gave positive mucosal staining. The staining was similar to that obtained with sera from patients with ulcerative colitis or from rats immunized with rabbit colon. No antibodies were found in the sera of germfree rats, germfree rats monocontaminated with various other bacteria, conventional rats of germfree origin, or conventional Sprague-Dawley rats. Although the anti-colon antibodies of the Clostridium infected rats reacted with the same feces extract as the antibodies of ulcerative colitis patients or of rabbit colon immunized rats, their specificity was different. While the latter cross-react with polysaccharide from E. coli O14, those from the Clostridium-infected exgermfree rats did not. Rats monocontaminated with Cl. difficile also developed antibodies to this organism, but no cross-reaction between Cl. difficile antigen and colon antigen could be demonstrated. This speaks against breakage of tolerance by cross-reacting bacterial antigen as the cause of autoimmunity in these rats. Other possible mechanisms for autoantibody production in this model are immunogenic alteration of gastrointestinal mucins by bacterial degradation, adjuvant effects of bacterial products, or both.

Animals↗
PubMed1969

Cytotoxic effects of leukocyres triggered by complement bound to target cells.

Chromium-51-labeled chicken erythrocytes (E), treated with rabbit anti-Forssman antibody (A) and the first four (C1-4) or the first seven (C1-7) components of human complement (C), released isotope upon exposure to human leukocytes. Isotope release from EACJ-7 cells proceeded more rapidly and was more extensive than that from EACI-3 cells. Lysis of these cells was suppressed by pretreatment of leukocytes with antimycinA. Monocyte-enriched leukocyte preparations affected both types of target cell-complement intermediates, whereas purified lymphocytes lysed EACI-7 cells but not EACI-3 cells.

Animals↗