Our data suggest that this occurs around the time of onset of joint pathology (days 20–25) as in the early stages, both systemically and locally in the joint, IL‐17 and IL‐22 (in the relatively low levels at which they are present) appear to act cooperatively (and may indeed both be derived from Th17 cells as described for IL‐1–driven arthritis [45]) to promote pathogenesis, whereas in the IL‐22–mediated protection phase, IL‐17 levels are high and IL‐17 and IL‐22 appear to be produced by antagonistic cell populations. This evidence concerns the gene IL17A and arthritic joint disease.