IgE and inflammatory cells: the cellular networks in allergy.
The expression by macrophages, eosinophils, and platelets of IgE receptors (Fc epsilon RII) confers on these cells, present or recruited at the site of allergen challenge, a direct role in the development of adverse allergic reactions. The IgE-dependent activation of macrophages, eosinophils, and platelets is moreover inhibited by antiallergic drugs such as disodium cromoglycate or nedocromil. This network of IgE-dependent effector cells is controlled by immunoregulatory pathways which can be target of desensitization therapy. Contrary to their deleterious role in allergic disorders, IgE- and Fc epsilon RII-bearing cells play a decisive role in the immune defense against helminth parasites, therefore pointing to a dualistic function of IgE.
Dessaint
J P
JP
Centre d'Immunologie et de Biologie Parasitaire, Unité Mixte INSERM U167-CNRS 624, Institut Pasteur, Lille, France.
Capron
A
A
D000944:Antigens, Differentiation, B-Lymphocyte / Q000502:physiology; D004804:Eosinophils / Q000502:physiology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007073:Immunoglobulin E / Q000502:physiology*; D007249:Inflammation / Q000276:immunology*; D008262:Macrophage Activation; D010272:Parasitic Diseases / Q000276:immunology; D015539:Platelet Activation; D011961:Receptors, Fc / Q000502:physiology; D017455:Receptors, IgE
D000944:Antigens, Differentiation, B-Lymphocyte; D011961:Receptors, Fc; D017455:Receptors, IgE; D007073:Immunoglobulin E