Suppression of inflammation and joint destruction in rheumatoid arthritis may require a concerted action of Th2 cytokines.

A predominance of T-helper 1 (Th1) activity and a lack of Th2 activity has been documented in the inflamed joints of patients with rheumatoid arthritis (RA). This imbalance is suggested to contribute to activation of, particularly, inflammatory macrophages and B-cells. Th2-mediated immunity, like atopy, is associated with amelioriated inflammation and joint damage in RA patients. Despite the potent anti-inflammatory capacities of two prominent Th2 cytokines in many experimental studies, clinical trials with either human IL-4 or IL-10 in RA patients did not lead to substantial disease suppression. Based on a thorough evaluation of the actions of IL-4 and IL-10 in these studies, it is hypothesized that disease suppression of RA may require the concerted action of suppressive Th2 cytokines or Th2 activity.