The p19 subunit was abundantly expressed in RA but not in OA synovial tissues. p19 was most prominently expressed by RASF in the synovial lining layer and at the site of invasion, but no heterodimeric IL23 was detected at these sites.
Since the IL-23/IL-17 pathway is known to associate with other autoimmune diseases, including rheumatoid arthritis (RA) and systemic sclerosis (SSc), we hypothesised that IL-23R could be a shared susceptibility gene.
Thus, controlling IL-23 production and function could be a strategy for preventing inflammation and bone destruction in patients with rheumatoid arthritis.
Low levels of wild-type (wt)COUP-TFI transgene expression did not inhibit neural cell fate and primarily enhanced neuron outgrowth from RA-treated P19 aggregates.
Following an analysis of the types of cells and antibodies found in joints affected by rheumatoid arthritis, it is concluded that both expression of oncogenes and the presence of retroviral sequences detectable by monoclonal antibodies to HTLV I p19 and p24 sequences are associated with early abnormal proliferation of apparently transformed cells at the site of initial cartilage and/or bone destruction.