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Streptococcal Cell Wall Antigens and Rheumatoid Arthritis

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Rheumatoid Arthritis

Abstract

Although detailed mechanistic questions still remain, Group A streptococci are the established causative agents of rheumatic fever and poststreptococcal reactive arthritis [4, 14, 18]. The possibility exists that streptococcal or related bacterial antigens are the etiologic agents in some cases of adult or juvenile forms of rheumatoid arthritis. Indeed, a large body of data in support of this hypothesis demonstrates that cell walls from selected types of streptococci and other bacteria are potent inducers of experimental rheumatoid arthritis-like disease in certain strains of rats [11, 58, 59, 60, 62, 64]. Additional data link streptococcal cell wall proteins and related bacterial substances to rheumatoid factor production [9, 32, 42, 58]. Accordingly, this review will summarize some of the more recent information on these issues.

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Authors and Affiliations

  1. Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Building 10, Room 9N240, Bethesda, Maryland, 20892, USA

    L. J. Crofford & R. L. Wilder

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  1. L. J. Crofford
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  2. R. L. Wilder
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Editors and Affiliations

  1. 2. Medizinische Abteilung Zentrum fü Diagnostik und Therapie rheumatischer Erkrankungen, Krankenhaus der Stadt Wien-Lainz und Ludwig Boltzmann Institut für Rheumatologie und Balneologie, Wolkersbergenstraße 1, A-1130, Wien, Austria

    Josef S. Smolen

  2. Medizinische Klinik III mit Poliklinik und Institut für Klinische Immunologie und Rheumatologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Krankenhausstraße 12, W-8520, Erlangen, Germany

    Joachim R. Kalden

  3. Mathilda and Terence Kennedy Institute of Rheumatology, 6 Bute Gardens, W6 7DW, Hammersmith, London, UK

    Ravinder N. Maini

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Crofford, L.J., Wilder, R.L. (1992). Streptococcal Cell Wall Antigens and Rheumatoid Arthritis. In: Smolen, J.S., Kalden, J.R., Maini, R.N. (eds) Rheumatoid Arthritis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76189-8_14

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