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Editorial
. 2019 Sep;71(9):1396-1399.
doi: 10.1002/art.40879. Epub 2019 Aug 1.

New Relationships for Old Autoantibodies in Rheumatoid Arthritis

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Editorial

New Relationships for Old Autoantibodies in Rheumatoid Arthritis

Miriam A Shelef. Arthritis Rheumatol. 2019 Sep.
No abstract available

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Figures

Figure 1.
Figure 1.. Two models for interactions between the shared epitope, smoking, ACPAs, and RF.
A. In the convergent pathways model, one of two converging pathways consists of antigen presenting cells (APCs) presenting citrullinated peptides (green) on shared epitope (SE)-containing MHC class II molecules to activate T cells. Those T cells then provide help to citrulline-reactive B cells to generate anti-citrullinated protein antibodies (ACPAs) of the IgG isotype. In the second of two converging pathways, smoking drives IgM-rheumatoid factor (RF) producing B cells. These pathways converge with RF+ B cells binding ACPA immune complexes to present citrullinated antigen via MHC to activate more citrulline-reactive T cells. Those T cells activate more citrulline reactive B cells leading to more ACPAs. Additionally, activated citrulline-reactive T cells can provide help to IgM-RF producing B cells that bind ACPA immune complexes to generate IgG-RF. B. In the common antigen model, citrullinated IgG (green) is bound by IgM-RF producing B cells, which then present citrullinated IgG peptides via shared epitope containing MHC class II to citrulline-reactive T cells. Those T cells then provide help to citrullinated IgG-binding B cells leading to IgG that targets citrullinated IgG and could be called both an ACPA and a RF.

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