SummaryInfective larvae of Brugia pahangi were injected subcutaneously into inbred PVG (‐RIT) rats, and ‘nude’ (PVG ‐rnu/rnu) (athymic) rats. Adult worms or circulating microfilariae were recovered from 20/34 (59%) of PVG ‐RTICrats and from 30/30 (100%) of ‘nude’ rats. Fertile worms were regularly found in the lumbar lymphatics and hearts of both strains of rat. Blood eosinophilia first developed in PVG ‐RTIcrats about 17 days, and in all such animals by 6 weeks. High circulating eosinophil counts persisted only in patent animals, proving a useful hallmark for the presence of microfilariae. Nude rats despite patency, developed eosinophilia only latterly and then to a lesser extent. Specific anti‐2?. pahangi IgG antibody was first detected at 7 days in all infected PVG ‐RTT rats, with levels rising until 8 weeks and remaining high only in microfilaraemic animals; total IgE showed a similar response. Specific IgE rose in all the eight patent rats inconsistently and only to low levels in eight non‐patent infected rats. IgG and IgE were undetectable in nude rats. Other strains of inbred rats of different RTI haplotype were also successfully infected with B. pahangi and the human parasite B. malayi, a total of 10/23 (43%) and 5/15 (33%) becoming patent respectively. In the small numbers tested no major influence of RTI haplotype was detected. Infection by the intraperitoneal route did not result in the development of microfilariae. The difference in patency rates between ‘nude’ and normal PVG rats supports the contention that the development of filarial infections is T lymphocyte dependent. Inbred and ‘nude’ rats provide a valuable model of human filariasis, in which many features of filarial i