Mechanisms of protective immunity to larvae of Brugia pahangi were studied in congenitally athymic nude C3H/HeN mice and their syngeneic heterozygous littermates. An average 11% if subcutaneous larval inocula was recovered from control nudes 28 days after inoculation. No worms were recovered from nude recipients of viable splenic Thy 1·2+ T lymphocytes from heterozygotes which had killed a priming does of B. pahangi larvae. Primed T lymphocytes, depleted of either Lyt 1·1+of Lyt 2·1+cells or incubated with anti-Thy 1.2 monoclonal antibody and complement, failed to protect nude mic against a larval challenge. Nor were primed B lymphocytes depleted by Thy 1·2+T cell contaminants protective. Treatment with cyclosporin A (CsA) did not increase the numbers of worms recovered from heterozygotes nor did CsA treatment of heterozygous cell donor abolish the ability of primed Thy 1·2+T lymphocytes to transfer protection to nude mice. IgG but not IgM antibody titres to B. pahangi antigens were depressed in all CsA-treated mice. CsA treatment of nude mice had no direct effect upon development of B. pahagi larvae. These results show that ptotective immunity to larvae of B. pahangi in mice depends upon small numbers of Thy 1·2+T cells which are CsA-resistant.