Recent studies of the major cell types involved in the initiation and progression of allergic inflammation have revealed that they express an unexpectedly large number of surface receptors that inhibit the release of proinflammatory mediators from mast cells and basophils in vitro. Moreover, analyses of animals deficient in some of these receptors, for example, FcγRIIB, gp49B1 and paired Ig-like receptor (PIR)-B, have shown that the molecules indeed suppress allergic responses driven by the adaptive immune response in vivo. These findings support the emerging concept that allergic diseases are caused not only by excessive activation of cells but also from deficiencies in receptors that suppress these activation responses.