Study of procainamide hapten-specific antibodies in rabbits and humans

Adams, Louis E.; Roberts, Stephen M.; Donovan-Brand, Rebecca; Zimmer, H.; Hess, Evelyn V.

doi:10.1016/0192-0561(93)90006-k

Cited by 14 publications

(6 citation statements)

References 36 publications

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“…Any of these changes may generate neo-antigenic determinants, and frequently antibodies raised against peptides with minor structural modification can also show cross-reactivity with the native protein, thus exhibiting true autoreactivity with self [10]. Neo-antigenic determinants may also arise from environmental damage such as UV exposure [14] and as a side effect from therapeutic drugs, such as procainamide [14], which can lead to adduct formation with self-antigens.…”

Section: Generation Of Neo-antigenic Determinantsmentioning

confidence: 99%

Is the generation of neo-antigenic determinants by free radicals central to the development of autoimmune rheumatoid disease?

Griffiths¹

2008

Autoimmunity Reviews

115

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Biomolecules are susceptible to many different post-translational modifications that have important effects on their function and stability, including glycosylation, glycation, phosphorylation and oxidation chemistries. Specific conversion of aspartic acid to its isoaspartyl derivative or arginine to citrulline leads to autoantibody production in models of rheumatoid disease, and ensuing autoantibodies cross-react with native antigens. Autoimmune conditions associate with increased activation of immune effector cells and production of free radical species via NADPH oxidases and nitric oxide synthases. Generation of neo-antigenic determinants by reactive oxygen and nitrogen species ROS and RNS) may contribute to epitope spreading in autoimmunity. The oxidation of amino acids by peroxynitrite, hypochlorous acid and other reactive oxygen species (ROS) increases the antigenicity of DNA, LDL and IgG, generating ligands for which autoantibodies show higher avidity. This review focuses on the evidence for ROS and RNS in promoting the autoimmune responses observed in diseases rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). It considers the evidence for ROS/RNS-induced antigenicity arising as a consequence of failure to remove or repair ROS/RNS damaged biomolecules and suggests that an associated defect, probably in T cell signal processing or/or antigen presentation, is required for the development of disease.

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Section: Generation Of Neo-antigenic Determinantsmentioning

confidence: 99%

Is the generation of neo-antigenic determinants by free radicals central to the development of autoimmune rheumatoid disease?

Griffiths¹

2008

Autoimmunity Reviews

115

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“…Drug-induced lupus is generally assumed to result from interactions between the drug or its metabolite and an element of the immune system. Despite several attempts to detect a direct stimulatory effect of PAHA on lymphocytes (9,38) or autoantibody production (39), no or only marginal changes have been reported. In the present study, PAHA also showed no capacity to directly activate the established peripheral immune system since injection of PAHA in the spleen or the peritoneal cavity had no detectable effect.…”

Section: Discussionmentioning

confidence: 99%

Autoimmunity caused by disruption of central T cell tolerance. A murine model of drug-induced lupus.

Kretz-Rommel¹,

Duncan²,

Rubin³

1997

J. Clin. Invest.

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“…Several lines of evidence suggest a role for oxidative stress in the pathogenesis of RA [133–139]. Epidemiologic studies have shown an inverse association between dietary intake of antioxidants and RA incidence [140–143], and, reciprocally, an inverse association between antioxidant levels and inflammation [39, 144, 145]. Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen (such as superoxide and peroxides), and a natural byproduct of the normal metabolism of oxygen.…”

Section: Antioxidized Protein Antibodies In Ramentioning

confidence: 99%

Autoantibodies to Posttranslational Modifications in Rheumatoid Arthritis

Burska

Hunt

Boissinot

et al. 2014

Mediators of Inflammation

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Autoantibodies have been associated with human pathologies for a long time, particularly with autoimmune diseases (AIDs). Rheumatoid factor (RF) is known since the late 1930s to be associated with rheumatoid arthritis (RA). The discovery of anticitrullinated protein antibodies in the last century has changed this and other posttranslational modifications (PTM) relevant to RA have since been described. Such PTM introduce neoepitopes in proteins that can generate novel autoantibody specificities. The recent recognition of these novel specificities in RA provides a unique opportunity to understand human B-cell development in vivo. In this paper, we will review the three of the main classes of PTMs already associated with RA: citrullination, carbamylation, and oxidation. With the advancement of research methodologies it should be expected that other autoantibodies against PTM proteins could be discovered in patients with autoimmune diseases. Many of such autoantibodies may provide significant biomarker potential.

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Study of procainamide hapten-specific antibodies in rabbits and humans

Cited by 14 publications

References 36 publications

Is the generation of neo-antigenic determinants by free radicals central to the development of autoimmune rheumatoid disease?

Is the generation of neo-antigenic determinants by free radicals central to the development of autoimmune rheumatoid disease?

Autoimmunity caused by disruption of central T cell tolerance. A murine model of drug-induced lupus.

Autoantibodies to Posttranslational Modifications in Rheumatoid Arthritis

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