Finfish in the wild are regularly subjected to low temperatures, which have been shown to cause a loss of Major Histocompatibility receptor expression in common carp kept at 6 degrees C. This is similar to what was seen in a mammalian cell line cultured at 26 degrees C. Loss of expression of this critical viral recognition protein may provide one mechanism for the increased frequency of fish diseases at low temperatures. This report demonstrates that unlike carp and mammals, beta(2)m transcript levels in both rainbow trout and Atlantic salmon do not decrease after 10 days at temperatures as low as 2 degrees C. Reverse transcriptase (RT)-PCR indicated that transcript steady-state levels of trout beta(2)m were maintained in both tissues and peripheral blood leucocytes, whether freshly isolated or in primary culture. Polyclonal antibodies raised against a recombinant form of trout beta(2)m, demonstrated cross-reactivity to both rainbow trout and Atlantic salmon protein lysates. Use of these antibodies in western blot analyses indicated that cellular protein levels are also maintained at low temperatures in both species while qualitative epifluorescence analysis of freshly isolated peripheral blood leucocytes indicated persistent cell surface expression of trout beta(2)m even after 10 days at 2 degrees C. Rainbow trout and Atlantic salmon may therefore utilise an alternative mode of immune gene regulation than the common carp and mammals allowing them to maintain viral recognition machinery at low temperatures, possibly due to selection for survival in cold climates.