Horbach, E.

Kaiser, Doris

Otte, M.

Rögener, W.

Scriba, Peter Christian

Stöcker, W.

English

Open Access LMU ( Ludwig-Maximilians-Univ. München)

Immunobiology Zeitschrift für Immunitätsforschung Editors E. D . ALBERT, München • D . BITTE R-Su ERMANN, Hannover • M . P. D l ER I 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 l m • E. K L E I N , Stockholm • W. K Ö H L E R , Jena • U . KOSZINOWSKI, U l m • P. KRAMMER, Heidelberg • M . LOOS, Mainz • T. LüGER, 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 . PF1ZENMAIER, Göttingen • M . RöLLINGHOFF, Erlangen • D . SCHENDEL, 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 . WEKERLE, Martinsried • G. W l C K , Innsbruck • R. ZlNKERNAGEL, Zürich Editor-in-Chief D . GFALSA, 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 O E H M E R , Basel • G. B O N N A R D , Bern • D . G. B R A U N , Basel • V. B R A U N , Tübingen • J . BROSTOFF , 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 KOR, Basel • P. ERB, Basel • H . - D . FLAD, Borstel • O . G Ö T Z E , Göttingen • E. GÜNTHER, Göttingen • U . H A D D I N G , Mainz • H . H A H N , Berlin • K. HÄLA, Innsbruck • G. J. H Ä M M E R L I N G , Heidelberg • K. U . H A R T M A N N , Marburg • H . ZUR HAUSEN, Heidelberg • M . HESS, Bern • J. K A L D E N , Erlangen • T. J. K I N D T , New York • E. K O W N A T Z K I , Freiburg • \V. LEIBOLD, Hannover • K. LENNERT, Kiel • F. LILLY, New York • J. L l N D E M A N N , Zürich • E. M A C H E R , Münster • H . M E T Z G E R , Bethesda • V. T E R M E U L E N , Würzburg • H . J . MÜLLER -EBERHARD, Hamburg • W. MÜLLER-RUCHHOLTZ, Kiel • H . PETERS, Göttingen • E. PlCK, Tel Aviv • O. P R O K O P , Berlin • M . Q U A S T E L , 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 l L L , Ann Arbor • G. U H L E N B R U C H , Köln • M . W A G N E R , Jena • P. W E R N E T , Düsseldorf D 00 SEMPER 2 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, TGF-ß . . . . 13 Interferon production, leukotriene C 4 . . 40 3 5 7 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 N o n - 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 ß2-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 267 220 • XXIst Meeting of the Society of Immunology Department of Medicine, Medical University of Lübeck, and E U R O I M M U N , Lübeck, FRG J.10 Detection of autoantibodies against exocrine pancreas by double immunodiffusion testing W I E B K E RÖGENER, W . STÖCKER, M . O T T E , E. H O R B A C H , D O R I S KAISER, and P. C. SCRIBA Autoantibodies against a component of pancreatic juice (PAb) occur in 39 % of patients w i t h Crohn's disease (CD) , as determined by indirect immunofluorescence ( I IF ; 1). In the XXIs t Meeting of the Society of Immunology • 221 present study double immunodiffusion ( D I D ) testing was used as an alternative method for the detection of PAb, and results were compared to those of I IF . Serum samples from 70 patients with C D were tested, 35 of which were PAb-positive in I IF , the other 35 were PAb-negative. Furthermore, 35 sera from patients wi th different diagnoses were used which were PAb-negative in I I F . D I D was performed with 1 % agarose gels in 0.1 M Tris buffer, p H 8.0, containing 2.5 % polyethyleneglycol 6000. Monoclonal antibody H L - 1 to PAg was used as a positive control . PAg was enriched from homogenized human pancreas by size exclusion chromatography and ammonium sulphate precipitation. Gels were incubated for 7 days at 4°C, dried and stained w i t h Serva blue R. O f 35 sera positive in I IF , 30 showed clear precipitation lines. In 2 other cases precipitation was only weak. Three IIF-positive samples did not react in D I D . A l l sera which were negative in I I F were negative in D I D . Reactions of identity were seen with most positive sera, but 5 precipitation lines crossed over, indicating that autoantibodies to exocrine pancreas may react wi th different epitopes or even different components of the crude antigen preparation used. The epitopes recognized by H L - 1 seemed to be different f rom those reacting w i t h PAb of serum samples. Despite long incubation times, D I D is a convenient, easy to handle complementary method for the detection of autoan-tibodies against exocrine pancreas which enables the diagnosis of many cases of C D in laboratories where I IF testing is not established. 1. STÖCKER, W . et al. 1987. Scand. J. Gastroenterol. 22 Suppl. 139: 41-52. 

Detection of autoantibodies against exocrine pancreas by double immunodiffusion testing

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Detection of autoantibodies against exocrine pancreas by double immunodiffusion testing

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