A comparative study of peritoneal mast cells from mutant IL-4 deficient and normal mice: evidence that IL-4 is not essential for mast cell development but enhances secretion via control of IgE binding and passive sensitization.

IL-4 enhances the growth and secretory function of mouse connective tissue type mast cells in vitro. To examine further the mast cell regulatory role of IL-4 we compared certain phenotypic and functional characteristics of peritoneal mast cells from mutant IL-4 deficient (IL-4(-/-)) or normal wildtype (IL-4(+/+)) mice. No differences were seen between mast cells from the two types of mouse in terms of numbers, histamine content, cell size, ultrastructure and number and size of granules. Mast cells from IL-4 deficient or wildtype mice responded equally to specific IgE/antigen and IL-4. However, Fc epsilon RI of IL-4(-/-) (in contrast to wildtype) mast cells were not pre-loaded with IgE, which would be expected to facilitate passive sensitization. Moreover, the in vitro total IgE binding capacity of mutant mast cells was significantly less than that of wildtype. Further in vitro experiments showed that IL-4 selectively enhanced IgE/antigen- rather than anti-IgE-induced degranulation from normal mast cells, and this effect was accompanied by an IL-4 induced increase in IgE binding capacity. In conclusion, IL-4 is not essential for peritoneal mast cell growth and exocytosis but regulates secretion via control of IgE binding and sensitization.