Inhibition of proliferation of mouse T cell-dependent bone marrow-derived mast cells by rat serum does not change their unique phenotype.

Both mouse and rat sera have been found to inhibit proliferation in vitro of interleukin 3-dependent chondroitin sulfate E proteoglycan-containing mouse bone marrow-derived mast cells (BMMC), as assessed by quantitation of 3H-labeled thymidine incorporation into DNA, cell cycle analysis, and cell number. Rat serum (9%) inhibited 3H-labeled thymidine incorporation within 60 min of exposure in a culture medium composed of 1% fetal calf serum (FCS) and 16% concanavalin A splenocyte-conditioned medium. The anti-proliferative effect of rat serum did not alter cell viability for 17 hr of subsequent culture, was dose related, with a maximal effect at 7% rat serum, and was reversible. Cytofluorographic analysis of relative DNA content per cell revealed that the proportion of cells in the S + G2 + M phases of the cell cycle was decreased in cells treated with 9% rat serum compared with cells cultured in either 1% or 10% FCS. These rat serum-treated BMMC exhibited no change in plasma membrane antigen phenotype as assessed by 15 monoclonal antibodies, and continued to synthesize chondroitin sulfate E proteoglycan. When sensitized with monoclonal IgE antibody, washed, and challenged with specific antigen, the rat serum-treated BMMC released the preformed secretory granule-associated mediators beta-hexosaminidase and histamine, and the newly generated lipid mediators leukotriene C4 (LTC4) and leukotriene B4 (LTB4) in amounts comparable to BMMC cultured in 10% FCS. Thus, the unique cell surface phenotype, the presence of chondroitin sulfate E proteoglycan rather than heparin proteoglycan, and the generation of LTC4 and LTB4 in a ratio of approximately 6:1 upon perturbation of the IgE receptor are distinctive characteristics of the interleukin 3-dependent mouse BMMC subclass, and not a functional consequence of the rapid proliferation of the cell.