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Pathogenesis

Yan Z, Aydelotte T, Gadi VK et al. Arthritis Rheum 2011;63:640–4.

This study reported that rheumatoid arthritis (RA) patients who were genotypically negative for the shared epitope (SE) could acquire the SE through microchimerism via fetal–maternal cell exchange, suggesting that SE-encoding microchimerism could contribute to the RA risk.

 

Human leukocyte antigen-DRB1*04 (HLA-DRB1*04) is associated with rheumatoid arthritis (RA) in the Caucasian population. HLA-DRB1*04 alleles encode similar sequences in the DRB1 third hypervariable region: QKRAA and QRRAA, which are known as the RA shared epitope (SE). However, a substantial number of RA patients lack the SE. In this study, the authors aimed to determine whether RA patients lacking HLA SE alleles can acquire the SE through microchimerism, a process involving bidirectional fetal–maternal trafficking.

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