Interleukin‐12 (IL‐12) responsiveness, and hence capacity to mount a T helper type 1(Th1) immune response, may be regulated via differential expression of the IL‐12 receptor β₂ subunit at least in vitro in human and murine cells. To test whether a similar phenomenon operates in vivo in the rat we cloned and sequenced partial cDNAs for rat IL‐12Rβ₁ and IL‐12Rβ₂ subunits and analysed expression of these genes in vivo in two rat strains with different Th1/Th2 bias. After treatment with mercuric chloride (HgCl₂), Brown–Norway rats develop Th2‐biased autoimmunity whereas Lewis rats do not develop autoimmunity, instead becoming resistant to Th1‐biased diseases to which they are normally susceptible. We report close sequence homology between the segments of the rat IL‐12R genes sequenced and corresponding mouse genes (95·6% and 92% for IL‐12Rβ₁ and IL‐12Rβ₂, respectively). Both Brown–Norway and Lewis rats express both β₁ and β₂ subunits of IL‐12 receptor in vivo in spleen; Brown–Norway rats express the β₂ subunit at a lower level than Lewis rats. After HgCl₂ treatment, IL‐12Rβ₁ expression was not altered but there was down‐regulation of IL‐12Rβ₂ expression in both strains. We conclude that relative under‐expression of IL‐12Rβ₂ by Brown–Norway rats contributes to their Th2 bias, and that down‐regulation of IL‐12Rβ₂ after HgCl₂ administration in Lewis rats underlies subsequent resistance to induction of Th1‐biased diseases.