The type III interferon (IFN) family comprises IFNλ1, IFNλ2 and IFNλ3, which are mainly known for their role in antiviral immunity. Now, Blazek et al. show that IFNλ2 has anti-inflammatory functions, and treatment with IFNλ2 halts and reverses the development of collagen-induced arthritis (CIA) in mice. After 4 days of IFNλ2 treatment — when progression of CIA was halted — the number of neutrophils was reduced in the joints of mice with CIA. This was associated with decreased levels of interleukin-1β, which is thought to be important for the amplification of CIA. Neutrophils expressed high levels of the IFNλ2 receptor, and the migration of these cells was restricted in response to IFNλ2. Interestingly, neutrophils are the most abundant immune cell in the synovial fluid of patients with rheumatoid arthritis. These results indicate that IFNλ2 or an IFNλ2 receptor agonist could be putative therapeutics for neutrophil-driven inflammation.