Figure 2: Contribution of autoreactive IgE to the pathogenesis of chronic spontaneous urticaria
Various autoallergens have been proposed to contribute to the pathogenesis of autoallergic CSU. These autoantigens are skin-derived, produced and released by lesional immune cells including basophils, eosinophils, Th2 cells, and macrophages/monocytes, or reach the tissue from the circulation. Autoallergens and IgE AAb may form immune complexes. Crosslinking of FcεRI by antigen-IgE complexes results in mast cell degranulation causing the typical signs and symptoms of CSU, i.e. itchy wheal and flare reactions and angioedema, as well as cytokine release causing further immune cell infiltration. In CSU, IgE AAb-driven reactions are primarily restricted to the skin presumably due to skin-prominent antigens and cross reactivity.
BAS: basophil, EOS: eosinophil, MC: mast cell, Mφ: macrophage, Mo: monocyte, Th2: CD4+ helper type 2 cells.