Abstract

Mast cells and basophils are important effector cells in T helper 2 (T_H2)-cell-dependent, immunoglobulin-E-associated allergic disorders and immune responses to parasites. The crosslinking of IgE that is bound to the high-affinity receptor FcRI with multivalent antigen results in the aggregation of FcRI and the secretion of products that can have effector, immunoregulatory or autocrine effects. This response can be enhanced markedly in cells that have been exposed to high levels of IgE, which results in the increased surface expression of FcRI. Moreover, recent work indicates that monomeric IgE (in the absence of crosslinking) can render mast cells resistant to apoptosis induced by growth-factor deprivation in vitro and, under certain circumstances, can induce the release of cytokines. So, the binding of IgE to FcRI might influence mast-cell and basophil survival directly or indirectly, and can also regulate cellular function.

Author affiliations

1. Division of Allergy, La Jolla Institute for Allergy and Immunology, 10355 Science Center Drive, San Diego, California 92121, USA.
2. Departments of Pathology, and Immunology and Microbiology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305-5324, USA.

Correspondence to: Stephen J. Galli² Email: sgalli@stanford.edu