The Pathogenesis of Chronic Spontaneous Urticaria: The Role of Infiltrating Cells

Chronic spontaneous urticaria is characterized by a perivascular non-necrotizing cellular infiltrate around small venules of the skin. It consists primarily of CD4(D) lymphocytes, a prominence of the T helper (Th)2 subtype but also Th1 cells, with Th17 cell-derived cytokines elevated in plasma. There are also neutrophils, eosinophils, basophils, and monocytes. Chemokines derived from mast cells and activated endothelial cells drive the process. Although the role of the cellular infiltrate has not previously been addressed, each constituent can contribute to the overall pathogenesis. It is of interest that CSU responds to corticosteroid, yet, short-term steroids do not affect autoimmunity or degranulation of mast cells, and act on margination of cells along the endothelium and chemotaxis to enter the surrounding dermis. In this review, we address each cell's contribution to the overall inflammatory response, as it is currently understood, with a view toward development of therapeutic options that impede the function of critical cells and/or their secretory products. (C) 2021 American Academy of Allergy, Asthma & Immunology

Automated summary

Chronic spontaneous urticaria is characterized by non-necrotizing cellular infiltrate around small skin venules, consisting primarily of CD4(D) lymphocytes, Th2 subtype, Th1 cells, and elevated Th17 cell-derived cytokines. Various cells, including neutrophils, eosinophils, basophils, and monocytes, contribute to the inflammatory response. While corticosteroids are effective in treating CSU, they primarily act on cell margination and chemotaxis rather than affecting autoimmunity or mast cell degranulation.