Abstract
In the present state of knowledge about the immunopathology of rheumatoid arthritis (RA), the failure to eliminate an unknown antigen has been postulated in several models. A defective macrophage function might be the cause of the persistence of non-degradable bacterial fragments (peptidoglycan) in the macrophage after successful phagocytosis and so produce a paradoxical hyperinflammatory response due to the continued existence of a positive tendency to inflammation1. In the infective theories, there is either short-term infection altering cells or tissue antigens and the infective agent then disappears leaving a self-perpetuating auto-immune response to altered self-antigens, or the infection can be persistent and is then responsible for perpetuation of pathology.
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Veys, E.M., Mielants, H. (1980). Review of immunotherapy in rheumatoid arthritis. In: Willoughby, D.A., Giroud, J.P. (eds) Inflammation: Mechanisms and Treatment. Inflammation: Mechanisms and Treatment, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-9423-8_8
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DOI: https://doi.org/10.1007/978-94-010-9423-8_8
Publisher Name: Springer, Dordrecht
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