BALB/c mice were inoculated subcutaneously with 400 third-stage infective larvae of N. brasiliensis (Nb) and the duration of infection, changes in the mesenteric lymph node (MLN) and spleen cell number and size, cell surface (s) IgD, IgM, IgE, and Thy-1.2, and intracytoplasmic (c) IgE were studied. Adult worms were cleared from the intestine of infected mice by 10 days after inoculation (DAI). Between 6 and 16 DAI there was a 2 to 4-fold increase in the cell number and the percentage of large cells in both MLN and spleen. The percentage of cIgE+ cells increased from undetectable levels in uninfected mice to as high as 0.5 to 1.0% in both the MLN and spleen of infected mice. Analysis of cell surface molecules with a fluorescence-activated cell sorter (FACS) revealed that Nb infection induced slight increases in the percentages of B cells and slight decreases in the percentages of T cells in MLN and spleen. More remarkably the percentages of sIgE+ cells in Nb-infected mice rose from undetectable levels to 35 to 40% of MLN and spleen cells. Analysis of MLN cells with a dual parameter FACS revealed that at the peak of the response almost all sIgD+ and sIgM+ lymphocytes were sIgE+, whereas few if any T cells bore sIgE. Treatment of MLN cells from Nb-infected mice with pH 4.0 acetate buffer for 1 min removed all detectable sIgE from more than 90% of sIgE+ cells but did not remove the sIgE from cIgE+ cells or sIgD or sIgM from cells with these surface isotypes. These data indicate that Nb infection is a potent stimulator of the murine IgE immune system and that it (1) induces a small, but considerable percentage of MLN and spleen B cells to acquire intrinsic sIgE and to synthesize large quantities of IgE, and (2) causes the majority of splenic B cells and almost all MLN B cells to acquire cytophilic sIgE. [AS]