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Rheumatoid factors in subacute bacterial endocarditis and other infectious diseases
1Department of Medicine, University of Florida, Gainesville 32610.
Abstract:
Rheumatoid factors (RF) occur during the course of various infections such as leprosy, infective endocarditis, tuberculosis, trypanosomiasis, visceral larva migrans, infectious mononucleosis, influenza A, hepatitis A or cytomegalovirus. When first described it seemed logical to assume that host-self-immunization with autologous immune complexes provided the initial stimulus for RF production. Subsequently extensive characterization of bacterial, parasitic and viral Fc receptors has suggested an alternative explanation for rheumatoid factor associated with infections. It seems possible that patients make an initial immune response to infecting agent Fc receptors and that anti-anti-Fc receptors or anti-idiotypes either then directly stimulate rheumatoid factor production or are themselves rheumatoid factors. Such a hypothesis might also be applied to rheumatoid arthritis itself where either infecting agent or autologous cell Fc receptors could be the initial immunizing epitopes involved in rheumatoid factor production.
Insights
Rheumatoid factors (RF) can arise from infections. An alternative hypothesis suggests RF production is triggered by immune responses to pathogen Fc receptors, potentially explaining RF in rheumatoid arthritis.
Area of Science:
- Immunology
- Infectious Diseases
- Rheumatology
Background:
- Rheumatoid factors (RF) are observed in various infections like tuberculosis and hepatitis.
- Previously, RF production was thought to stem from host self-immunization with immune complexes.
- Recent findings on microbial Fc receptors offer a new perspective on RF development.
Purpose of the Study:
- To explore an alternative hypothesis for rheumatoid factor production in infectious diseases.
- To investigate the role of Fc receptors from infectious agents in stimulating RF.
- To propose a unifying hypothesis for RF in both infections and rheumatoid arthritis.
Main Methods:
- Review of existing literature on rheumatoid factors and Fc receptors.
- Analysis of immune responses to microbial Fc receptors.
- Hypothetical modeling of RF generation pathways.
Main Results:
- Infectious agents possess Fc receptors that can elicit immune responses.
- Anti-Fc receptor antibodies or anti-idiotypes may stimulate RF production.
- This mechanism could also explain RF in rheumatoid arthritis via autologous Fc receptors.
Conclusions:
- Infections may trigger rheumatoid factor production through immune responses to microbial Fc receptors.
- This Fc receptor-centric hypothesis offers a potential explanation for RF in rheumatoid arthritis.
- Further research is warranted to validate the role of Fc receptors in RF pathogenesis.