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3. IX Eular Workshop for Rheumatology Research: Molecular biology of autoantigens, autoantibodies and immunopeptides. Vienna, Austria, March 9–12, 1989

Author

Fournier, C., Texier, B., Chiocchia, G., Boissier, M. C., Herbage, D., Brown, C. M. S., Zyberk, C. Plater, Maini, R. N., Palacios, A., Sieper, J., Heinegard, D., Panayi, G. S., Gentric, A., Mackenzie, L., Lydyard, P. M., Youinou, P., Menzel, E. J., Kaik, B., Sykulev, Yu. K., Guschin, A. Je., Vasiljev, V. I., Ostreiko, K. K., Yeronina, T. V., Tumanova, I. A., Moynier, M., Abderrazik, M., Combe, B., Rucheton, M., Brochier, J., Tuomi, T., Palosuo, T., Heliövaara, M., Aho, K., McHugh, N. J., James, I. E., Kallenberg, C. G. M., Tervaert, J. W. Cohen, Goldschmeding, R., Von Dem Borne, A. E. G. K. R., Bouanani, M., Piechaczyk, M., Pau, B., Bastide, M., Le Page, S., Williams, W., Parkhouse, D., Cambridge, G., Isenberg, D. A., Nimmegeers, J., De Keyser, F., Verbruggen, G., Veys, E. M., Walravens M. J. F., Verdeyen I., Vandepol B., Cortens W., Schatteman, L., Goethals, K., Wu, D. -H., Tavoni, A., Neri, R., Garzelli, C., Vitali, C., Bombardieri, S., Logar, D., Kveder, T., Dobovisek, J., Rozman, B., Menard, H. A., Boire, G., Lopez-Longo, F. J., Masson, Ch., Lapointe, S., Clair, E. W. St., Zerva, L., Moutsopoulos, H. M., Keene, J. D., Pisetsky, D. S., Van Dam, A. P., Cuypers, H. T. M., Winkel, I., Smeenk, R. J. T., Taylor, D., Valente, E., Foster, J. P., Williams, D. G., Stocks, M. R., Caporali, R., De Gennaro, F., Cerino, A., Cobianchi, F., Astaldi-Ricotti, G. C. B., Montecucco, C., Habets, W., Sillekens, P. T. G., Hoet, M. H., McAllister, G., Lerner, M. R., Van Venrooij, W. J., Habets, W. J., Van Der Kemp, A., De Jong, B., Scarpa, R., Pucino, A., Di Girolamo, C., della Valle, G., Larizza, G., Casiere, D., Oriente, P., Paimela, L., Palvimo, J., Kurki, P., Hassfeld, W., Steiner, G., Graninger, W., Smolen, J. S., Lopez-Longo, E. J., Larose, A., Hoet, R., Zewald, R., Smeenk, R., Brinkman, K., Van Den Brink, H., Westgeest, A., Huss, R., Krapf, E. F., Herrmann, M., Leitmann, W., Kalden, J. R., Merétey, K., Cebecauer, L., Böhm, U., Kozakova, D., Brózik, M., Temesvári, P., Nagy, L., Bozic, B., Stegnar, M., Vene, N., Peternel, P., Giuggioli, C., Monti, P., Rossi, G., Ferri, C., Chiellini, S., Baboonian, C., Venables, P. J. W., Roffe, L., Booth, J., Krapf, F., Abuljadayel, I., Ebringer, A., Cox, N. L., Brand, S. R., McIntosh, D. P., Bernstein, R. M., Van Den Broek, M. F., Van Bruggen, M. C. J., Smetsers, T., Kuyer, P., Van De Putte, L., Van Den Berg, W. B., Toivanen, A., Jalkanen, S., Lahesmaa-Rantala, R., Isomäki, O., Pekkola-Heino, K., Merilahti-Palo Saario, R., Von Essen, R., Isomäki, H., Granfors, K., Gaston, J. S. H., Life, P. F., Bailey, L., Bacon, P. A., Khalafpour, S., Wilson, C., Awad, J., Toivanen, P., Saario, R., Skurnik, M., Van Der Straeten, C., Mielants, H., Gazic, M., Hartung, K., Riedel, T., Stannat, S., Specker, Ch., Röther, E., Pirner, K., Schendel, D., Baur, M., Corvetta, A., Peter, H. H., Lakomek, H. J., Deicher, H., Andonopoulos, A. P., Papasteriades, C. A., Drosos, A. A., Dimou, G. S., Shattles, W., Venables, P., Charles, P. J., Markwick, J. R., Venables, P. J., Galeazzi, M., Lulli, P., Tuzi, T., Cappellacci, S., Morellini, M., Trabace, S., Cutrupi, F., Sorrentino, R., Botti, S., Iannicola, C., Costanzi, S., Tosi, R., Gospodinoff, A., Eliaou, J. F., Humbert, H., Balaguer, P., Nicolas, J. C., Sany, J., Clot, J., Sakkas, L. I., Bird, H., Welsh, K. I., Pitzalis, C., Kingsley, G., Haskard, D., Vischer, T. L., Bas, S., Werner-Favre, C., Wohlwend, D., Zubler, R. H., Afeltra, A., De Pita, O., Basso, P., Pietrucci, A., Ferri, G. M., Bonomo, L., Gerli, R., Cernetti, C., Bertotto, A., Agea, E., Arcangeli, C., Lanfrancone, L., Rambotti, P., Crupi, S., Baglioni, A., Spinozzi, F., Papazoglou, S., Skoumi, D., Athanasiou, P., Iliopoulos, A., Stavropoulou, A., Kontomerkos, T., Hendrich, G., Kuipers, J. G., Hammer, M., Schmidt, R. E., Manoussakis, M. N., Germandis, G., Zerva, L. V., Siouna-Fatourou, H. J., Katsikis, P. D., Mavridis, A., Toubert, A., Sadouk, M., de la Tour, B., Vaquero, C., Amor, B., Miossec, P., Naviliat, M., Cretien, I., Banchereau, J., Graninger, P., Aschauer, B., Sinski, A., Smolen, J., Krutmann, J., Kirnbauer, R., Köck, A., Schwarz, T., May, L. T., Sehgal, P. B., Luger, T. A., Field, M., Chu, C. Q., Feldmann, M., Wilbrink, B., Nietfeld, J. J., Helle, M., Boeije, L. C. M., Van Roy, J. L. A. M., Den Otter, W., Aarden, L. A., Huber-Bruning, O., Malejczyk, J., Urbanski, A., Malejczyk, M., Karbowski, A., Völker, W., Feige, U., Otter, W. Den, Malfait, A. M., Wieme, N., Gyselbrecht, L., Van de Loo, A. A. J., Van Lent, P. L. E. M., Haskard, D. O., Wellicome, S., Lanchbury, J., Thornhill, M., Krutmann, K., Gschnait, F., Yaron, M., Yaron, I., Dayer, J. -M., Bleiberg, I., Meyer, F. -A., Maury, C. P. J., Teppo, A. -M., Salo, E., Pelkonen, P., Malfait, A., Cochez, Ph., Gruschwitz, M., Müller, P. U., Wick, G., Madhok, R., Wilson, R., Frame, M., Thompson, J., Sturrock, R. D., Partsch, G., Matucci-Cerinic, M., Marabini, S., Jantsch, S., Neumüller, J., Eberl, R., van Beuningen, H. M., Arntz, O. J., Zlabinger, G. J., Steffen, C., Brand, H. S., Van Kampen, G. P. J., De Koning, M. H. M. T., Kiljan, E., Van Der Korst, J. K., Gemmell, C. G., Swaak, A. J. G., Van Rooyen, A., Hall, N. D., Woolf, A. D., Kantharia, B., Maymo, J., Blake, D. R., Goulding, N. J., Maddison, P. J., Munthe, E., Berntzen, H. B., Fagerhol, M., Mathieu, A., Pala, R., Contu, L., Cirillo, R., Garau, P., Nurchis, P., Viberti, G. C., Meyer, O., Zenklusen, C., Le Thi Huong Du, Z., Gaudouen, C., Mery, J. Ph., Ronco, P., Kahn, M. F., Rasmussen, N., Szpirt, W., Thomsen, B., Humbel, R. L., Ter Borg, E. J., Horst, G., Hummel, E., Limburg, P. C., Aeschilmann, A., Bourgeois, P., De Rooij, D. J., Van de Putte, L. B. A., Verbeek, L., Farinaro, C., Infranzi, E., Couret, M., Ackerman, C., De Vlam, K., Carapic, V., Carapic, D., Annefeld, M., Erne, B., Rosenwasser, L. J., Pazoles, C. J., Otterness, I. G., Hanson, D. C., McDonald, B., Loose, L. D., Dougados, M., Machold, K. P., Wiesenberg-Böttcher, I., Wanner, K., Pignat, W., Altmann, H., Tuschl, H., Bröll, H., Balestrieri, G., Tincani, A., Cattaneo, R., Bertoli, M. T., Martinelli, M., Allegro, F., Meroni, P. L., Balesini, G., Aichinger, G., Schlögl, E., Huber, Ch., Shoenfeld, Y., Fleishmaker, E., Mendlovic, S., Mozes, E., Blank, M., Talal, N., Hogervorst, E. J. M., Van Eden, W., Van Der Zee, R., Psychos, D., Dimou, G., Stefanaki-Nikou, S., Papadimitriou, C. S., Settas, L., Alexiou, P., Dimitriadis, G., Mataftsi, E., Soliou, E., Tourkantonis, A., Babic, M., Jeurissen, M. E. C., and Boerbooms, A. MTh

Published
1989
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8. Decreased Staining of Heparan Sulfate in Non-lesional Skin of a Subgroup of Patients with Systemic Lupus Erythematosus.

Author

Seyger, M. M. B, van Bruggen, M. C. J., Hardeman, H. K, van den Hoogen, F. H. J, Berden, J. H. M, van den Born, J, and de Jong, E. M. G. J

Subjects
*PROTEOGLYCANS, *IMMUNOHISTOCHEMISTRY techniques, *SYSTEMIC lupus erythematosus, *ANALYTICAL chemistry
Abstract

Heparan sulfate proteoglycans (HSPGs) are components of the basement membrane of various tissues. They are composed of a core protein and of the negatively charged glycosaminoglycan side chain heparan sulfate, which is covalently bound to the core protein. We previously found that in both human and murine lupus nephritis, heparan sulfate staining in the basement membrane of the glomerulus is almost completely absent, and that there was an inverse correlation between heparan sulfate staining and glomerular immunoglobulin deposits. As immunoglobulin deposits are also present in the skin of systemic lupus erythematosus patients, we investigated the heparan sulfate staining pattern in the basement membrane of the dermal-epidermal junction. Furthermore, we studied whether there was a correlation between heparan sulfate staining and deposition of immunoglobulin in the basement membrane of this junction, and between heparan sulfate staining and the presence of anti-DNA antibodies in the serum. Biopsies of non-lesional skin of 21 systemic lupus erythematosus patients (15 anti-DNA positive and 6 anti-DNA negative patients at the time of biopsy) were stained for the HSPG-core protein (mAb JM-72), highly sulfated stretches within heparan sulfate (JM-13), the low sulfated regions of heparan sulfate (mAb JM-403) and for immunoglobulin depositions. Abnormal and discontinuous staining of the low sulfated parts of heparan sulfate using mAb JM-403 in the basement membrane was found in skin biopsies of 4 out of 15 systemic lupus erythematosus patients with anti-DNA antibodies. In contrast, all specimens of anti-DNA negative patients showed normal continuous staining. Staining with JM-13 and JM-72 showed normal linear staining in both groups. The decreased heparan sulfate staining was correlated significantly with the presence of immunoglobulin deposits in the basement membrane. The subgroup could not be identified by its clinical picture. Our results suggest similar but not identical pathways in systemic lupus erythematosus nephritis and skin of systemic lupus erythematosus patients. [ABSTRACT FROM AUTHOR]

Published
1998
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9. Characterization of Two Fc Receptors for Mouse Immunoglobulins on Human Monocytes and Cell Lines.

Author

van de Winkel, J. G. J., Tax, W. J. M., van Bruggen, M. C. J., van Roozendaal, C. E. P., Willems, H. W., Vlug, A., Capel, P. J. A., and Koene, R. A. P.

Subjects
T cells, IMMUNOGLOBULIN G, CELL proliferation, LEUCOCYTES, CELL culture, LYMPHOCYTES, MOLECULAR cloning
Abstract

We have previously reported a polymorphism in the mitogenic effect of murine (m) IgGI anti-CD3 monoclonal antibodies. This polymorphism was genetically determined and could be attributed to polymorphism of the Fc receptor (FcR) for mIgGl present on human monocytes. We have now extended these studies by quantitating FcR expression on monocytes and cell lines by it recently developed EA rosette assay, using the erythrocyte-associated pseudoperoxidase activity. The data show that the polymorphism of the monocyte FcR for mIg2a-based on a quantitative rather than an absolute difference. Furthermore, this FcR is specific for mIgGI and does not bind mIgG2a nor mIgG2b nor surprisingly, human IgG. The expression of this FcR on cell lines correlates with their accessory function in IgG I anti-CD3-induced T cell proliferation mIgG2a can inhibit the rosetting of monocytes with erythrocytes sensitized with human IgG. The FcR detected by this rosette technique can interact with all four human IgG subclasses but not with mIgG1 or mIgG2b. The expression of this type of FcR in human cell lines correlates well with their ability to support mIgG2a anti-CD3-induced mitogenesis. These direct measurements of FcR expression support the concept that human monocytes have two independent FcR with affinity for mouse IgG: one receptor specific for mIgG2a (which also binds human IgG), and a second specific for mIgG1. [ABSTRACT FROM AUTHOR]

Published
1987
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10. Higher anti-heparan sulphate reactivity during systemic lupus erythematosus (SLE) disease exacerbations with renal manifestations; a long term prospective analysis.

Author

Kramers, C., Termaat, R. M., Ter Borg, E. J., van Bruggen, M. C. J., Kallenberg, C. G. M., and Berden, J. H. M.

Subjects
DNA antibodies, SYSTEMIC lupus erythematosus, AUTOIMMUNE diseases, IMMUNOGLOBULINS, HISTONES, NUCLEOPROTEINS, HEPARIN, IMMUNE complexes
Abstract

Cross-reactive antibodies against heparan sulphate (HS) have been suggested to play a role in initiating renal disease in SLE. Recently, we found that HS-reactivity is mediated by anti-DNA antibodies complexed with DNA and histones. To evaluate the clinical significance of anti-HS reactivity, we studied prospectively a cohort of 72 consecutive SLE patients, of whom 22 experienced 40 exacerbations. In 20 of these exacerbations renal symptoms were present. In these 20 exacerbations significantly higher anti-DNA (median 1: 160) and anti-HS (median 1: 30) titres were detected compared with exacerbations without renal manifestations (median 1:60 for anti-DNA and negative for anti-HS). There were no correlations with other symptoms of SLE. Anti-HS titres showed a significant correlation with anti-DNA antibody titres (rs = 0.57, P < 0.05). Anti-HS without anti-DNA reactivity was never detected. Some SLE patients showed a high anti-DNA titre without anti-HS reactivity, suggesting that not all anti-DNA antibodies are able to bind to histone/DNA complexes and thus to exhibit anti-HS reactivity. Our findings indicate that anti-HS reactivity is correlated with renal disease in SLE. [ABSTRACT FROM AUTHOR]

Published
1993
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