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[Pathophysiology of urticaria].

A Nosbaum1, F Augey2, J-F Nicolas3

  • 1Service 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.

Annales De Dermatologie Et De Venereologie
|December 26, 2014
PubMed
Summary
This summary is machine-generated.

Urticaria, a skin condition, involves mast cell activation leading to histamine release and edema. Diverse immunological and non-immunological pathways contribute to its varied symptoms and treatment responses.

Keywords:
HistamineHypersensibilitéHypersensitivityMast cellMastocytePathophysiologyPhysiopathologieUrticaireUrticaria

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Area of Science:

  • Immunology
  • Dermatology
  • Pathophysiology

Background:

  • Urticaria is characterized by dermal edema due to mast cell activation and mediator release, primarily histamine.
  • While histamine is a major mediator, other molecules like prostaglandins and cytokines contribute to urticaria's diverse clinical presentation.
  • Urticaria can be classified as immunological or non-immunological, involving complex hypersensitivity reactions or innate immunity pathways.

Purpose of the Study:

  • To explore the diverse pathophysiological mechanisms underlying urticaria.
  • To differentiate between immunological and non-immunological causes of mast cell activation in urticaria.
  • To highlight the heterogeneity of urticaria, influencing clinical manifestations and treatment outcomes.

Main Methods:

  • Review of immunological pathways including type I, II, III, and IV hypersensitivity reactions.
  • Analysis of non-immunological mast cell activation via innate immunity receptors and xenobiotics.
  • Correlation of pathophysiological mechanisms with clinical heterogeneity.

Main Results:

  • Immunoglobulin (Ig) G auto-antibodies binding to IgE or its receptor are implicated in autoimmune urticaria (up to 50% of chronic cases).
  • Type III hypersensitivity via immune complexes and type IV hypersensitivity involving T-cells also contribute to mast cell activation.
  • Non-immunological urticaria involves mast cell activation through innate immunity receptors or direct xenobiotic toxicity.

Conclusions:

  • Urticaria pathogenesis is multifactorial, involving various immunological and non-immunological pathways.
  • Understanding these diverse mechanisms is crucial for explaining the heterogeneity of urticaria symptoms and treatment responses.
  • Further research into these pathways can lead to more targeted and effective therapeutic strategies for urticaria.