A new model for an etiology of rheumatoid arthritis: smoking may trigger HLA-DR (shared epitope)-restricted immune reactions to autoantigens modified by citrullination.
By L. Klareskog, P. Stolt, K. Lundberg, H. Källberg, C. Bengtsson, J. Grunewald, J. Rönnelid, H. Harris, A. Ulfgren, S. Rantapää-Dahlqvist and 3 more. Arthritis & Rheumatism, 2006
1,587 citations recorded by the source corpus.
Subfields: Immunology, Pulmonary and Respiratory Medicine, Rheumatology
View Paper: https://www.semanticscholar.org/paper/9674c90db60ffc09da6e17f44ad09716ad79574b
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Citations in the corpus
- Rheumatoid arthritis: pathological mechanisms and modern pharmacologic therapies (2018, background): “Moreover, smoking in the context of the HLA-DR SE gene may trigger RA-specific immune reactions to citrullinated proteins.(34) DNA methylation mediates smoking and genotype interaction in ANPA-positive RA.”
- Peptidylarginine deiminase from Porphyromonas gingivalis citrullinates human fibrinogen and α-enolase: Implications for autoimmunity in rheumatoid arthritis (2010, background): “To date, tobacco exposure and the presence of certain alleles in the HLA-DRB1 locus with a common peptide-binding motif, collectively termed the ‘shared epitope’, have been identified as susceptibility factors for developing autoantibodies to citrullinated proteins (19,20), in particular α-enolase a”