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SUMMARYPregnancy is known to influence the course of rheumatoid arthritis (RA) in women, as well as type II collagen-induced arthritis (CIA) in DBA/I mice. A characteristic feature is the remission during gestation and the exacerbation ofthe diseases during the post-partum period. In the case of CIA in DBA/1 mice, two hormonal changes have been assumed to be critical for the induction of the postpartum flare: (i) the fall in steroid hormone levels from those present during pregnancy; and (ii) surges of prolactin (PRL) release at and after dehvery. Our results show that treatment with oestradio! during a short period immediately after parturition protects the mouse from a post-partum llare of the disease, and that treatment with bromocriptine. a drug known to inhibit the endogenous PRL release, has a significant though less marked effect. Studies of lactating (i.e. animals with physiological stimulation of endogenous PRL release) and non-lactating arthritic mice revealed no clear-cut differences, indicating that PRL is ofminor importance for the induction ofthe post-partum flare. Some steroids other than oestradiol. which may be implicated in the exacerbation of arthritis., namely progesterone and hydroeortisone. had no clinical eflect. Analyses of agalactosyl IgG levels in miee with CIA, and anti-eollagen II antibodies in sera collected at the end ofthe experiments revealed no significant differences between the oestradiol and the control groups. The suecessful oestradiol treatment ofthe mice indicates that the drop in endogenous oestradiol levels prior to delivery ends the oestrogen-mediated protection against arthritis during pregnancy.