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Autoimmunity and anti-TNF-alpha agents.

Abstract

Treatment of rheumatoid arthritis (RA) patients with anti-tumor necrosis factor-alpha (anti-TNF-alpha) biologic agents has been associated with a reduction in the levels of specific autoantibodies, such as rheumatoid factor (RF) and anticyclic citrullinated peptide (anti-CCP), and the induction of non- organ-specific autoantibodies (antinuclear antibodies [ANAs], anti-dsDNA, and antiphospholipid antibodies [aPLs]). The mechanisms by which the blockade of anti-TNF-alpha decreases the generation of specific autoantibodies, such as anti-CCP and RF, are not yet known. However, it has been shown that these agents can downregulate the production of several inflammatory cytokines and mediators and that these anti-inflammatory effects may account for reduced autoantibody generation, particularly in the synovial compartment. Infliximab treatment leads to the induction of ANAs in 63.8% of RA patients and 49.1% of Crohn's disease (CD) patients, and anti-dsDNA antibodies in 13% of RA patients and 21.5% of CD patients, respectively. The development of ANAs and anti-dsDNA antibodies has also been described after etanercept therapy in 11% and 15% of RA patients, respectively. In the controlled trials, increases in ANA and anti-dsDNA titers were observed in 5.3% and in 12.9% of adalimumab-treated RA patients. Only limited data on the induction of aPL antibodies during TNF-alpha blocking treatment are available.

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  • Authors+Show Affiliations

    ,

    Rheumatology Unit, Department of Rheumatology, University Hospital L Sacco, Via GB Grassi 74, 20157 Milan, Italy. sarzi@tiscali.it

    , , , ,

    Source

    MeSH

    Adalimumab
    Antibodies, Antinuclear
    Antibodies, Antiphospholipid
    Antibodies, Monoclonal
    Antibodies, Monoclonal, Humanized
    Arthritis, Rheumatoid
    Autoantibodies
    Autoimmunity
    DNA
    Etanercept
    Humans
    Immunoglobulin G
    Infliximab
    Peptides, Cyclic
    Receptors, Tumor Necrosis Factor
    Rheumatoid Factor
    Tumor Necrosis Factor-alpha

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    16126996

    Citation

    Atzeni, Fabiola, et al. "Autoimmunity and anti-TNF-alpha Agents." Annals of the New York Academy of Sciences, vol. 1051, 2005, pp. 559-69.
    Atzeni F, Turiel M, Capsoni F, et al. Autoimmunity and anti-TNF-alpha agents. Ann N Y Acad Sci. 2005;1051:559-69.
    Atzeni, F., Turiel, M., Capsoni, F., Doria, A., Meroni, P., & Sarzi-Puttini, P. (2005). Autoimmunity and anti-TNF-alpha agents. Annals of the New York Academy of Sciences, 1051, pp. 559-69.
    Atzeni F, et al. Autoimmunity and anti-TNF-alpha Agents. Ann N Y Acad Sci. 2005;1051:559-69. PubMed PMID: 16126996.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Autoimmunity and anti-TNF-alpha agents. AU - Atzeni,Fabiola, AU - Turiel,Maurizio, AU - Capsoni,Franco, AU - Doria,Andrea, AU - Meroni,Pierluigi, AU - Sarzi-Puttini,Piercarlo, PY - 2005/8/30/pubmed PY - 2006/6/27/medline PY - 2005/8/30/entrez SP - 559 EP - 69 JF - Annals of the New York Academy of Sciences JO - Ann. N. Y. Acad. Sci. VL - 1051 N2 - Treatment of rheumatoid arthritis (RA) patients with anti-tumor necrosis factor-alpha (anti-TNF-alpha) biologic agents has been associated with a reduction in the levels of specific autoantibodies, such as rheumatoid factor (RF) and anticyclic citrullinated peptide (anti-CCP), and the induction of non- organ-specific autoantibodies (antinuclear antibodies [ANAs], anti-dsDNA, and antiphospholipid antibodies [aPLs]). The mechanisms by which the blockade of anti-TNF-alpha decreases the generation of specific autoantibodies, such as anti-CCP and RF, are not yet known. However, it has been shown that these agents can downregulate the production of several inflammatory cytokines and mediators and that these anti-inflammatory effects may account for reduced autoantibody generation, particularly in the synovial compartment. Infliximab treatment leads to the induction of ANAs in 63.8% of RA patients and 49.1% of Crohn's disease (CD) patients, and anti-dsDNA antibodies in 13% of RA patients and 21.5% of CD patients, respectively. The development of ANAs and anti-dsDNA antibodies has also been described after etanercept therapy in 11% and 15% of RA patients, respectively. In the controlled trials, increases in ANA and anti-dsDNA titers were observed in 5.3% and in 12.9% of adalimumab-treated RA patients. Only limited data on the induction of aPL antibodies during TNF-alpha blocking treatment are available. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/16126996/full_citation L2 - https://doi.org/10.1196/annals.1361.100 DB - PRIME DP - Unbound Medicine ER -