Horbach, E.

Kaiser, D.

Otte, M.

Rögener, W.

Scriba, Peter Christian

Stöcker, W.

English

Open Access LMU

Immunobiology Zeitschrift für Immunitätsforschung Editors E. D . A L B E R T , München • D . B lTTER -SUERMANN, Hannover • M . P. D l E R l C H , Innsbruck • M . F E L D M A N N , London • S. H . E. K A U F M A N N , U lm • E. K L E I N , Stockholm • W. K Ö H L E R , Jena • U . K O S Z I N O W S K I , U lm • P. K R A M M E R , Heidelberg • M . L O O S , Mainz • T. L U G E R , Münster • L . J. O L D , New York • J. J. O P P E N H E I M , Frederick • H . H . PETER, Freiburg • K. P F I Z E N M A I E R , Göttingen • M . R Ö L L I N G H O F F , Erlangen • D . S C H E N D E L , München • V. SCHIRRMACHER, Heidelberg • C. SORG, Münster • R. V A N F U R T H , Leiden • H . W A G N E R , München • H . W E K E R L E , Martinsried • G. W l C K , Innsbruck • R. ZlNKERNAGEL, Zürich Editor-in-Chief D. GEMSA, Marburg Editorial Advisory Board R. A V E R D U N K , Berlin • J. F. B A C H , Paris • H . B A L N E R , Rijswijk • R. B E N N E R , Rotterdam • H . v. B OK H M ER, Basel • G. BONNARD, Bern • D . G. B R A U N , Basel • V. BRAUN, Tübingen • J. BROSTOII-, London • A. C O U T I N H O , Paris • T. D I A M A N T S T E I N , Berlin • W . D R Ö G E , Heidelberg • P. D U K O R , Basel • P. ERB, Basel • H . - D . FLAD, Borstel • O . GÖTZE, Göttingen • E. GÜNTHER, Göttingen • U . H A D D I N G , Mainz • H . H A H N , Berlin • K. H Ä L A , Innsbruck • G . J. H A M M KR L I N G , Heidelberg • K. U . H A R T M A N N , Marburg • H . ZUR HAUSEN, Heidelberg • M . HESS, Bern • J. KALDEN, Erlangen • T. J. K I N D T , New York • E. KOWNATZKI , Freiburg • \V. L E I B O L D , Hannover • K. L E N N E R T , Kiel • F. L I L L Y , New York • J. L I N D E M A N N , Zürich • E. MACHER, Münster • H . METZGER, Bethesda • V. TER MEULEN, Würzburg • H . J. MÜLLER -EBERHARD, Hamburg • W. MÜLLER-RUCHHOLTZ, Kiel • H . PETERS, Göttingen • E . PlCK, Tel Aviv • O. PROKOP, Berlin • M . QUASTEL, Beer Sheva • J. P. REVILLARD, Lyon • E. P. RlEBER, München • E. RÜDE, Mainz • E . SCHÖPF, Freiburg • H . G. SCHWICK, Marburg • K. SETHI, Heidelberg • G. SUNSHINE, London • N . T A L A L , San Francisco • G. T I L L , Ann Arbor • G. U H L E N B R U C K , Köln • M . WAGNER, Jena • P. WERNET, Düsseldorf D m SEMPER m Gustav Fischer Verlag • Stuttgart • New York • 1990 Subject Index Activation, tumor-associated macrophages Active ulcerative colitis, p - A N C A . . . . Adenylate cyclase, regulation Alveolar leukocytes, hyporesponsive-ness Alveolar leukocytes, interferon inducers . Anti-self reactivity, M H C class I genes . Antibody-forming cells, intestinal antigen A u t o - M H C Class II-reactive T cell line . Autoimmune thyroiditis BCG-immunized mice, interferon-y pro-duction Borrelia burgdorferi associated antigens, monoclonal antibodies C D 4 + lymphocyte dynamics, H I V infected individuals C D 8 + cells, hemorrhaged mice Chondrocytes, Mycoplasma arthritidis . Colony stimulating activity, Hodgkin's disease Crohn's disease, p - A N C A Cyclophosphamide-induced tolerance . . Cyclosporins A, granulocyte function . . Dendritic cell-associated molecule . . . . Dendritic cells, H L A class I I molecules . Endothelial cells, tumor necrosis factor-a Endotoxin administration, neopterin levels Exocytosis, nucleotide-induced Granulocyte function, cyclosporins A . . Granulocytes and endothelial cells, tumor necrosis factor-a Granulocytes, monoclonal antibody . . . Hemorrhaged mice, transfer of T cells . . Hepatitis virus type 3, age-dependent resistance Hepatitis virus type 3, macrophage activation H I V infected individuals, C D 4 + dynamics H I V infected individuals, C D 4 + 276 dynamics 108 406 H L A class I I molecules, dendritic cells . . 335 51 H L A class I I molecules, monocytes . . . 335 H L A - B 8 , D R positive individuals, 84 T lymphocyte activation 257 84 Hodgkin's disease, colony stimulating 438 activity 288 Hybridoma suppressor factor (HSF) . . . 64 97 3 6 7 IL-1 receptor 13 4 1 4 IL-2 receptor 13 IL-2 , suppressor cells 345 Indomethacin, suppressor cells 345 40 Inhibit ion of proliferation, T G F - ß . . . . 13 Interferon production, leukotriene C 4 . . 40 357 Interferon-a inducers, alveolar leukocytes 84 Interferon-y inducers, alveolar leukocytes 84 Intestinal antigen, antibody-forming 398 c e l l s 9 7 288 Leukotriene C 4 , interferon production . . 40 406 L p r - G V H D , characterization 367 430 Lymphoki ne production, hybridoma 22 suppressor factor (HSF) 64 Macrophage activation, hepatitis virus 335 r y p e 3 3 1 Macrophage activation, interferon-y . . . 31 Macrophages, tumor-associated 276 M H C class I genes, anti-self reactivity . . 438 267 Model-based analysis, H I V infected individuals 108 3 1 7 Monoclonal antibodies, Borrelia 298 burgdorferi associated antigens . . . . 357 Monoclonal antibody, rat granulocytes . 324 22 Monocytes, H L A class I I molecules . . . 335 Monocytes, Hodgkin's disease 288 267 MRL/+mice 367 324 Mycoplasma arthritidis, T cell lines . . . 398 379 Neopterin levels, endotoxin administra-tion 317 31 Neutrophils, k i l l of tumor cells 1 Neutrophils, tumoricidal factor 1 31 NLDC-145 molecule, dendritic cell-associated 388 108 Non-H-2 alloantigen 430 460 • Subject Index p - A N C A , ulcerative colitis 406 Peyer's patches inactivation 97 Peyer's patches, antibody-forming cells . 97 Spontaneous autoimmune thyroiditis . . 414 Staphylococcal enterotoxin A , inter-feron-y production 40 Suppressor cells, effect of IL-2 345 Suppressor cells, effect of indomethacin . 345 ß 2 -adrenoceptors , regulation 51 f cell line, l p r - G V H D 367 T cell lines, Mycoplasma arthritidis . . . 398 T lymphocyte markers, H L A - B 8 , DR3 positive individuals 257 Tolerance, non-H-2-alloantigen 430 Transfer of T cells, hemorrhaged mice . . 379 Transforming growth factor-beta . . . . 13 Tumor cells, killed by neutrophils . . . . 1 Tumor necrosis factor-a, granulocytes and endothelial cells 267 Tumor-associated macrophages 276 Ultrastructural study, granulocytes and endothelial cells 267 234 • X X l s t Meeting of the Society of Immunology E U R O I M M and Department of Medicine, Medical University of Lübeck, FRG K. l 1 A fluorescent lectin-agarose bead immunoassay for a pancreatic autoantigen involved in Crohn's disease W I E B K E R Ö G E N E R , E. H O R B A C H , D O R I S KAISER, W . STÖCKER, M . O T T E , and P. C. SCRIBA Pancreatic autoantigen (PAg) which is recognized by many sera of patients with Crohn's disease (CD) could up to now only be identified by a neutralization technique, in which the capacity of samples to extinguish a specific immunofluorescence reaction of CD-sera wi th human pancreatic tissue sections was recorded. However, the neutralizing efficacy of crude duodenal juice or homogenized pancreas could not be evaluated, since activated proteinases digested the tissue sections. Solid phase immunotests, based on direct binding of PAg to plastic surfaces gave inconsistent results, possibly depending on the low affinity of PAg to the materials used. We have found out that PAg binds to soybean agglutinin (SBA) which is known to react wi th N-acetylgalactosamine. Thus, it was possible to develop a new assay for the detection of PAg: Samples were diluted in microtiter plates (50 ud per well) and incubated for 15 min with 10 u,l of a 50% suspension of SBA-coated agarose beads (Carrion, Wiesba-den). 50 uJ of 1 % ovalbumine were added. After washing in PBS, beads were further incubated wi th 50 ul of H L - 1 (monoclonal antibody against PAg; for 30 min, washed again and stained for 30 min wi th FITC-labelled goat anti-mouse IgG. Results were read wi th a fluorescence microscope. Positive beads exhibited a bright fluorescence. O f 200 samples which were identified to contain PAg as determined by the neutralization test, each was clearly positive in the lectin agarose bead immunoassay. Semiquantification was possible by titration of samples in twofold dilutions, which resulted in a clear cut end point. PAg could easily be detected in homogenized pancreas and contents of the bowel. The new assay for PAg was simple to perform, easy to read and seems to be more widely applicable than the neutralization test. 

A fluorescent lectin-agarose bead immunoassay for pancreatic autoantigen involved in Crohn´s disease

Universität München: Elektronischen Publikationen

http://epub.ub.uni-muenchen.de/8613/1/8613.pdf

A fluorescent lectin-agarose bead immunoassay for pancreatic autoantigen involved in Crohn´s disease

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Universität München: Elektronischen Publikationen