Despite extensive research, the cause of rheumatoid arthritis remains unknown. However, most doctors agree that a combination of genetic and environmental factors is responsible.
Over the past 20 years, and especially in the past year or two, progress has been made toward identifying genes linked to an increased risk of rheumatoid arthritis. One such factor found on the surface of white blood cells, or lymphocytes, is known as major histocompatability antigen, or human leukocyte antigen (HLA). The HLA genetic site, or locus, controls immune responses.
Researchers have shown that people with a specific genetic marker called the HLA shared epitope have a fivefold greater probability of developing rheumatoid arthritis than do people without the marker. Other more recently identified genes with a connection to RA include: STAT4, a gene that plays important roles in the regulation and activation of the immune system; TRAF1 and C5, two genes relevant to chronic inflammation; and PTPN22, a gene associated with both the development and progression of rheumatoid arthritis.
Yet not all people with these genes develop RA and not all people with rheumatoid arthritis have these genes, so researchers are investigating other factors that may play a role. Suspects include infectious agents such as bacteria or viruses, which may trigger development of the disease in someone who has the genetic propensity for it; female hormones (70 percent of people with RA are women) and the body’s response to stressful events such as physical or emotional trauma.
