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A new model for an etiology of rheumatoid arthritis: Smoking may trigger HLA–DR (shared epitope)–restricted immune reactions to autoantigens modified by citrullination

Arthritis & Rheumatism · 2005 · Vol. 54(1) · pp. 38–46
Lars KlareskogPatrik StoltKarin LundbergHenrik KällbergCamilla BengtssonJohan GrünewaldJohan RönnelidHelena Erlandsson HarrisAnn‐Kristin UlfgrenSolbritt Rantapää‐DahlqvistAnders EklúndLeonid PadyukovLars Alfredsson

Abstract

We identified an environmental factor, smoking, that in the context of HLA-DR SE genes may trigger RA-specific immune reactions to citrullinated proteins. These data thus suggest an etiology involving a specific genotype, an environmental provocation, and the induction of specific autoimmunity, all restricted to a distinct subset of RA.

Rheumatoid Arthritis Research and TherapiesSystemic Lupus Erythematosus ResearchViral Infections and Immunology ResearchCitrullinationImmunologyAutoimmunityRheumatoid arthritisMedicineAutoantibodyRheumatoid factorEpitopeImmune systemBronchoalveolar lavage

MeSH terms

AdolescentAdultAgedAntibodiesEpitopesArthritis, RheumatoidCitrullineFemaleHLA-DR AntigensHumansMaleMiddle AgedSmokingCase-Control Studies
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