Ultraviolet light-inactivated feline leukemia virus (FeLV) and its 15,000 dalton envelope protein (p15E) inhibited concanavalin A receptor motility of feline peripheral lymphocytes (PBL). In contrast, the virus had no effect on immunoglobulin capping of feline PBL. The inhibitory action of FeLV and FeLV p15E was reversed by the addition of indomethacin. The indomethacin effect was titratable and gave significant reversal between 1 X 10(-5) and 1 X 10(-10) M. The indomethacin inhibition of the prostaglandin synthesis does not appear to be the mechanism of action in its ability to reverse FeLV suppression of Con A receptor mobility. Since the addition of prostaglandin E2 (PGE2) (1.0 microM) was also able to reverse the FeLV-induced inhibition and neither indomethacin nor PGE2 had an observable effect on Con A receptor mobility of normal PBL without FeLV present. PBL from FeLV-infected cats were sensitive to indomethacin (1.0-10.0 microM) and an indomethacin-related increase in cap formation was observed. Since both indomethacin and PGE2 were able to reverse the FeLV-induced suppression it was concluded that their mechanism of action may be through a common site. In addition, indomethacin may prove useful as an immune response modifier for therapy in FeLV-infected cats.