Citrullination of autoantigens: upstream of TNFα in the pathogenesis of rheumatoid arthritis

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Citrullination of autoantigens : upstream of TNFα in the pathogenesis of rheumatoid arthritis. / Quirke, Anne-Marie; Fisher, Benjamin A C; Kinloch, Andrew J; Venables, Patrick J.

In: FEBS Letters, Vol. 585, No. 23, 01.12.2011, p. 3681-8.

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Quirke, Anne-Marie ; Fisher, Benjamin A C ; Kinloch, Andrew J ; Venables, Patrick J. / Citrullination of autoantigens : upstream of TNFα in the pathogenesis of rheumatoid arthritis. In: FEBS Letters. 2011 ; Vol. 585, No. 23. pp. 3681-8.

Bibtex

@article{1d364091f23f451f99bc1e584220f45a,
title = "Citrullination of autoantigens: upstream of TNFα in the pathogenesis of rheumatoid arthritis",
abstract = "Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by synovial inflammation and destruction of joints. Over 20 years ago, tumour necrosis factor alpha (TNFα) was identified as a key player in a cytokine network, whose multifunctional effects could account for both the inflammation and destruction in RA. The remarkable efficacy of TNF inhibitors in the treatment of RA has resulted in extensive research addressing the regulation of TNFα production responsible for this excessive production. The discovery of autoimmunity to citrullinated protein/peptide antigens (ACPA) has led the concept that ACPA may be the essential link between disease susceptibility factors and the production of TNFα, which ultimately accounts for the disease phenotype. In this review we will consider (1) the mechanisms of citrullination, both physiological and pathological, (2) how known genetic and environmental factors could drive this peculiar form of autoimmunity and (3) how the immune response could lead to excessive production of TNFα by the synovial cells and ultimately to the disease phenotype (Fig. 1).",
keywords = "Animals, Arthritis, Rheumatoid, Autoantibodies, Autoantigens, Citrulline, Humans, Models, Immunological, Tumor Necrosis Factor-alpha",
author = "Anne-Marie Quirke and Fisher, {Benjamin A C} and Kinloch, {Andrew J} and Venables, {Patrick J}",
note = "Copyright {\textcopyright} 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.",
year = "2011",
month = dec,
day = "1",
doi = "10.1016/j.febslet.2011.06.006",
language = "English",
volume = "585",
pages = "3681--8",
journal = "FEBS Letters",
issn = "0014-5793",
publisher = "Elsevier",
number = "23",

}

RIS

TY - JOUR

T1 - Citrullination of autoantigens

T2 - upstream of TNFα in the pathogenesis of rheumatoid arthritis

AU - Quirke, Anne-Marie

AU - Fisher, Benjamin A C

AU - Kinloch, Andrew J

AU - Venables, Patrick J

N1 - Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

PY - 2011/12/1

Y1 - 2011/12/1

N2 - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by synovial inflammation and destruction of joints. Over 20 years ago, tumour necrosis factor alpha (TNFα) was identified as a key player in a cytokine network, whose multifunctional effects could account for both the inflammation and destruction in RA. The remarkable efficacy of TNF inhibitors in the treatment of RA has resulted in extensive research addressing the regulation of TNFα production responsible for this excessive production. The discovery of autoimmunity to citrullinated protein/peptide antigens (ACPA) has led the concept that ACPA may be the essential link between disease susceptibility factors and the production of TNFα, which ultimately accounts for the disease phenotype. In this review we will consider (1) the mechanisms of citrullination, both physiological and pathological, (2) how known genetic and environmental factors could drive this peculiar form of autoimmunity and (3) how the immune response could lead to excessive production of TNFα by the synovial cells and ultimately to the disease phenotype (Fig. 1).

AB - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by synovial inflammation and destruction of joints. Over 20 years ago, tumour necrosis factor alpha (TNFα) was identified as a key player in a cytokine network, whose multifunctional effects could account for both the inflammation and destruction in RA. The remarkable efficacy of TNF inhibitors in the treatment of RA has resulted in extensive research addressing the regulation of TNFα production responsible for this excessive production. The discovery of autoimmunity to citrullinated protein/peptide antigens (ACPA) has led the concept that ACPA may be the essential link between disease susceptibility factors and the production of TNFα, which ultimately accounts for the disease phenotype. In this review we will consider (1) the mechanisms of citrullination, both physiological and pathological, (2) how known genetic and environmental factors could drive this peculiar form of autoimmunity and (3) how the immune response could lead to excessive production of TNFα by the synovial cells and ultimately to the disease phenotype (Fig. 1).

KW - Animals

KW - Arthritis, Rheumatoid

KW - Autoantibodies

KW - Autoantigens

KW - Citrulline

KW - Humans

KW - Models, Immunological

KW - Tumor Necrosis Factor-alpha

U2 - 10.1016/j.febslet.2011.06.006

DO - 10.1016/j.febslet.2011.06.006

M3 - Article

C2 - 21704035

VL - 585

SP - 3681

EP - 3688

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 23

ER -