In rheumatoid arthritis, immune cells called helper T cells behave differently from their counterparts in healthy cells and in other autoimmune diseases. Stanford scientists have learned why.
Stanford University School of Medicine investigators succeeded in countering inflammation and tissue damage caused by rheumatoid arthritis in mice engrafted with human joint-lining tissue and a human immune system.
The researchers accomplished this by shutting down a faulty molecular mechanism that they identified in humans with the disease.
A study led by Cornelia Weyand found that shutting down a faulty molecular mechanism in mice could curb the damage caused by rheumatoid arthritis.