To investigate mechanisms of mast-cell proliferation, we have utilized infection of Lewis rats with the intestinal nematode, Nippostrongylus brasiliensis, which induces a pronounced intestinal mast-cell hyperplasia. Adoptive transfer of 2 x 10(8) immune mesenteric lymph node cells (IMLN), collected 14 days post infection with 3000 third stage larvae (L3), into rats concurrently given 3000 L3 hastened the expected intestinal mastocytosis by up to 4-5 days. IMLN exhibited this mastopoietic activity in the presence but not in the absence of concurrent infection. Normal mesenteric lymph node cells did not show similar mastopoietic activity. Intestinal mastocytosis was delayed by sub-lethal irradiation (400 rad) but IMLN reconstituted the mast-cell response of such animals. The mastopoietic activity could not be attributed to worm antigen as antigen administered intravenously had no significant effect on mastocytosis and furthermore, antigen could not be detected in mastopoietically active IMLN suspensions used as a possible antigen source in passive cutaneous anaphylaxis tests. Immune serum (14 days post primary infection with 3000 L3) also hastened mastocytosis in infected rats, whereas normal serum did not. The IMLN may be an enriched source of intestinal mast cell precursors and, in addition, may contain a cell type(s) which regulates the differentiation and proliferation of such precursors.