Thursday, June 8, 2023
In accordance with ACCME Standards for Commercial Support of Continuing Medical Education and the Health Science Center for
Continuing Medical Education Disclosure Policy for CME Activities, faculty members have been asked to disclose any relationship
they may have with commercial supporters of this CME activity or with companies providing drugs, medical equipment, etc, that
may have relevance to the content of their presentations. Such disclosure is intended to provide participants with sufficient
information to evaluate whether any given presentation has been influenced by the faculty's relationship(s) or financial interests
with said companies.
The following faculty have reported receiving something of value from the commercial supporter(s) of this activity or from
a corporate organization whose product(s) may have relevance to the content of their presentations:
Professor, Academic Section of Musculoskeletal Disease, University of Leeds; Clinical Director, Department of Rheumatology, Leeds Teaching Hospitals NHS Trust, Leeds, England
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As suggested by RA concordance in twins in the previously described studies, the likelihood of developing RA is influenced to a significant degree by genetic factors. Polymorphisms of several genes that are important in the regulation of immune responses have been linked to an increased risk of developing RA. Many high-risk alleles have been identified in MHC class II genes, including HLA-DQB1, HLA-DQA1, and especially HLA-DRB1.[10] The HLA-DR4 region of the HLA-DRB1 gene cluster is strongly associated with an increased risk of severe and persistent RA.[10] The risk of RA associated with all of the high-risk HLA-DR4 alleles has been attributed to the presence of 1 of 3 specific amino acid sequences, comprising amino acids 70-74. These shared epitopes consist of various sequences of the amino acids glutamine (Q), leucine (K), arginine (R), and alanine (A): QKRAA, QRRAA, or RRRAA.[11] In monozygotic twins, the homozygous presence of either the QKRAA or QRRAA epitope in HLA-DR4 confers a 5-fold increase in the risk of developing RA.[12] Thus, it has been hypothesized that RA may be initiated when RA-associated MHC molecules present self-antigens to autoreactive T cells, although the antigens involved in this process have not been definitively identified.[10]
