• A Nosbaum, F Augey, J-F Nicolas, and F Bérard.
• Service d'Immunologie Clinique et Allergologie, Centre Hospitalier Lyon-Sud, 69495 Pierre Bénite cedex, France; UFR Médecine Lyon-Sud - Charles Mérieux, 165, Chemin du Petit Revoyet - BP 12, 69921 Oullins cedex, France; Université Claude Bernard Lyon 1, 43 Boulevard du 11 Novembre 1918, 69622 Villeurbanne cedex, France; Inserm U1111, Centre International de Recherche en Infectiologie (CIRI), UMS3444/US8, SFR BioSciences Gerland, 50 avenue Tony Garnier, 69366 Lyon cedex 7, France; University of California, San Francisco, Department of Dermatology, 513 Parnassus Avenue HSW-518, San Francisco CA 94143-0511, United States.
• Ann Dermatol Vener. 2014 Nov 1; 141 Suppl 3: S559-64.

AbstractUrticaria is a dermal edema resulting from vascular dilatation and leakage of fluid into the skin in response to molecules released from mast cells. The major mediator responsible for urticaria is histamine. However, the clinical spectrum and pattern of lesions indicate that other molecules, including prostaglandins, leukotrienes, cytokines, and chemokines, produced at different times after mast cell activation contribute to the polymorphism of this symptom and the variable evolution of this disease. It is a common practice to distinguish immunological and nonimmunological urticaria. Immunological urticaria is a hypersensitivity reaction mediated by antibodies and/or T-cells that results in mast cell activation. Although immunoglobulin (Ig) E-mediated type I hypersensitivity (HS) was long postulated to be the major immunological pathway associated with mast cell activation, interaction between IgEbound mast cells and allergens is unlikely to be the mechanism by which urticaria develops in most patients. It is now well established that urticaria may result from the binding of IgG auto-antibodies to IgE and/or to the receptor for IgE molecules on mast cells, thus corresponding to a type II HS reaction. These auto-immune urticarias represent up to 50 % of patients with chronic urticaria. Mast cell activation can also result from type III HS through the binding of circulating immune complexes to mast cell-expressing Fc receptors for IgG and IgM. Finally, under certain circumstances, T-cells can induce activation of mast cells, as well as histamine release (type IV HS). Nonimmunological urticarias result from mast cell activation through membrane receptors involved in innate immunity (e.g., complement, Toll-like, cytokine/chemokine, opioid) or by direct toxicity of xenobiotics (haptens, drugs). In conclusion, urticaria may result from different pathophysiological mechanisms that explain the great heterogeneity of clinical symptoms and the variable responses to treatment.Copyright © 2014 Elsevier Masson SAS. All rights reserved.

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