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.