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22. HLA typing in families with multiple cases of rheumatoid arthritis

Author

Strotzer, M., Menninger, H., Scholz, S., and Albert, E.D.

Subjects
HLA histocompatibility antigens -- Genetic aspects, Rheumatoid arthritis -- Physiological aspects, Health
Abstract

The HLA (human leukocyte antigen) system of cell-surface antigens (molecules capable of provoking an immune response) is similar to the blood group ABO antigens in that subtle differences in these molecules, coded for by the DNA in genes, identify an individual's cells as his own, immunologically speaking, and provoke graft rejection after transplantation. Certain HLA subgroups are strongly related to particular diseases, such as diabetes. Studies of some families have shown a relationship between frequent cases of rheumatoid arthritis (RA) and the subgroup HLA-DR4, while in some ethnic groups, HLA-DR1 is linked to RA instead. Whether the proteins made from the sequences of DR genes or the DR genes themselves are linked to other genes predisposing to RA is uncertain. Complete HLA typing was done in 31 RA patients from 14 families with multiple occurrences of RA, as well as in 42 healthy relatives. Class I antigens, HLA-A, -B, and -C were not more prevalent in patients. The class II antigens DR1 occurred in 32 percent of patients and in 12 percent of healthy subjects, while DR4 occurred in 48 percent and 28 percent, respectively, with the increased frequencies in patients being significant. These results were combined with those from other reports, and analysis revealed that DR1 and DR4 have a dominant influence in the inheritance of RA. The data suggest that some DR antigens may play a direct role in the development of RA. HLA antigens did not correlate with medical variables such as disease severity. Only 68 percent of the patients in this study had DR1 or DR4, suggesting that about one third of RA patients may have a type of disease which is independent of HLA factors. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

23. Third Eular Workshop on Rheumatology Research: Mainz February 1983

Author

Gleichmann, E., van Rappard-van der Veen, F. M., Rolink, A. G., Pals, S. T., Trautwein, G., Hewicker, M., Waterfield, J. D., Maini, R. N., Botzenhardt, U., Müller, J., Lemmel, E. -M., Bartlett, R., Steldern, D. v., Field, M., Schrieber, L., Melsom, R. D., Venables, P. J., McCarthy, D. A., de Vries, B. J., van den Berg, W. B., van de Putte, L. B. A., van den Berg, W. B., Lens, J. W., Kruijsen, M. W. M., Brackertz, D., Mohr, W., Fritsch, R., Holmdahl, R., Rubin, K., Klareskog, L., Radaszkiewicz, T., Dreher, R., Köhler, G., Rieber, P., Weber, U., Kirchhoff, H., Heitmann, J., Hermanns, W., Schulz, L. Cl., Marquardt, J., Rojem, P., Schulz, L. C., Brighton, S. W., Vermeulen, W. A., Madhok, R., Sturrock, R. D., Forbes, C., Bennett, D., Leibold, W., Hangoc, G., Böhm, K. H., Rimpler, M., Grabczewska, E., Maslinski, W., Krzystyniak, K., Ryzewski, J., Mbuyi, J. M., Dequeker, J., Junker, P., Oxlund, H., Lorenzen, G. H., Lorenzen, I., Van Paassen, H. C., De Vries, E., Mallee, C., Bijvoet, O. L. M., Cats, A., Ball, J., Wessinghage, D., Kirkpatrick, C. J., Verbruggen, G., Luyten, F., Veys, E. M., Annefeld, M., Velvart, M., Fehr, K., Seidel, J., Menninger, H., Gurr, E., Stangel, W., Deicher, H., Fobbe, C., Starck, P., Kleesiek, K., Greiling, H., Biemond, P., Swaak, A. J. G., Koster, J. F., Hall, N. D., Maslen, C., McKeown, M. J., Parnham, M. J., Bittner, C., Hurst, N. P., Bessac, B., Nuki, G., Neumüller, J., Dunky, A., Senautka, G., Eberl, R., Lemmel, E. M., Lindgren, J. A., Appelboom, T., Gortz, R., Madia, W., Loos, M., Heinz, H. P., Mortazavi-Milani, S. M., Holborow, E. J., Lindblad, S., Hedfors, E., Meijer, C. J. L. M., Lafeber, G. J. M., Vulpen-Cnossen, J., Damsteeg, W. G. M., Warnatz, H., Lemm, G., van der Weij, J. P., van der Veen, C. J. P., Burmester, G. R., Menche, D., Merryman, P., Dimitriu-Bona, A., Klein, M., Winchester, R., Corke, C. F., Gul, V., Stierle, H., Huskisson, E. C., Holborrow, E. J., Froebel, K., Dickson, R., Lewis, D., Kávai, M., Sonkoly, I., Csongor, J., Szegedi, Gy., Schmidt, R. E., Mollenhauer, E., Heinrichs, M., Rittner, C., Schneider, E. M., Pawelec, G., Müller, C., Blaurock, M., Shaw, S., Wernet, P., Winrow, V. R., Stierle, H. E., Norton, J., March, R. E., Santana, R., Deycke, K. H., Baruth, B., Weibbarth, E., Zeller, H., Ebringer, A., Geissler, N., Hildebrand, S., Kemper, A., Krapf, E., Renger, D., Schedel, I., Zeidler, H., Mielke, H., Krauledat, P. B., Krapf, F. E., Baudner, S., Linhart, H., Kalden, J. R., Maddison, P. J., Skinner, R. P., Esscher, E., Taylor, P. V., Scott, O., Scott, J. S., Miossec, P., Youinou, P., Le Goff, P., Seigneurin, J. M., Coatalem, R., Trautmann, F., Arnold, W., Hermanns, Ph., Delanghe, J., Vansteenkiste, M., Mielants, H., Munthe, E., Jellum, E., Suykens, S., Schiller, H., Schilling, F., and Emrich, E.

Published
1983
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44. Expression of the CD2 Activation Epitope T11‐3 (CD2R) on T Cells in Rheumatoid Arthritis, Juvenile Rheumatoid Arthritis, Systemic Lupus Erythematosus, Ankylosing Spondylitis, and Lyme Disease: Phenotypic and Functional Analysis

Author

POTOCNIK, A. J., primary, MENNINGER, H., additional, YANG, S. Y., additional, PIRNER, K., additional, KRAUSE, A., additional, BURMESTER, G. R., additional, BRÖKER, B. M., additional, HEPT, P., additional, WESELOH, G., additional, MICHELS, H., additional, TRUCKENBRODT, H., additional, EMMRICH, F., additional, and KROCZEK, R. A., additional

Published
1991
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