Interleukin‐11 (IL‐11) is a cytokine belonging to the IL‐6 family which has both pro‐ and anti‐inflammatory potential. Like IL‐6 it can diminish tumour necrosis factor‐α and IL‐1 production, and augment immunoglobulin synthesis. We have explored the immunomodulatory effects of IL‐11 treatment in mice in a model of inflammatory autoimmune joint disease, collagen‐induced arthritis (CIA). Recombinant human IL‐11 was administered at various doses to DBA/1 mice after the onset of CIA. IL‐11 treatment caused a significant reduction in the clinical severity of established CIA, which was associated with protection from joint damage, as assessed by histology. Although there was a suggestion at high doses of IL‐11 that the anticollagen type II (CII) response may have been augmented, there was no statistically significant effect of IL‐11 treatment on anti‐CII antibody levels. Similarly, the acute‐phase reactant serum amyloid P was only elevated in mice receiving very high doses (50–100 μg/day) of IL‐11. Endogenous IL‐11 was abundantly produced in synovial membrane cultures derived from CII‐immunized mice with active disease, suggesting that, as in rheumatoid arthritis, this cytokine is spontaneously produced in the inflammatory response in CIA. The results presented here demonstrate an anti‐arthritic immunoregulatory role for IL‐11 in murine CIA, and suggest that IL‐11 is a candidate therapeutic molecule for human inflammatory arthritic diseases.