Salvatore Albani, M.D., Ph.D, professor of medicine and pediatrics and Director of the Translational Research Unit of the Clinical Investigation Institute (CII) at the UCSD School of Medicine, recently presented a summary of the findings at the "Frontiers of Clinical Investigation Symposium." The symposium, sponsored by the CII and Nature Medicine, was held in La Jolla, California in September.
The new drug, dnaJP1, is a peptide derived from a naturally occurring protein, dnaJ, which generates inflammation in RA patients, whose inflammatory-control mechanisms are impaired. The impairment causes the body's T cells which trigger inflammation to kill and clear foreign pathogens in the body to attack the body's own tissues.
"In essence, we re-educated the immune system T cells to be tolerant of the dnaJP1 amino acid sequence, which would usually contribute to inflammation in rheumatoid arthritis patients," Albani said.
DnaJP1 works by resetting the ability of the patient's immune system to tolerate dnaJ, thus transforming a potentially damaging trigger into a tool for controlling the disease. Oral ingestion of dnaJP1 is key, because the mucosal immune system found in the gut has the ability to "teach" the body to view a protein as one that isn't dangerous or foreign. Much as food is ingested into the body and not rejected, the body tolerates dnaJP1.
Current medications for treating RA range from anti-inflammatory drugs, such as aspirin, to corticosteroids and medicines that alleviate symptoms by suppressing or killing the body's immune response, basically crippling the body's ability to defend itself against other infectious diseases or cancer.