Advances in allergic skin diseases Donald Y.M. Leung, MD, PhDa, Mark Boguniewicz, MDb  Journal of Allergy and Clinical Immunology  Volume 111, Issue 3, Pages S805-S812 (March 2003) DOI: 10.1067/mai.2003.155 Copyright © 2003 Mosby, Inc. Terms and Conditions

Fig. 1 Functional autoantibodies of CIU. IgG anti-IgE antibodies combine with and cross-link adjacent receptor-bound IgE. IgG anti-FcϵRI antibodies combine with and cross-link adjacent α-chains of FcϵRI. Black notched membrane structures represent α-chain of FcϵRI expressed on surface of dermal mast cell. From Greaves M. Chronic urticaria. J Allergy Clin Immunol 2000;105:664-72. Used with permission. Journal of Allergy and Clinical Immunology 2003 111, S805-S812DOI: (10.1067/mai.2003.155) Copyright © 2003 Mosby, Inc. Terms and Conditions

Fig. 2 Aberrant regulation of the p21Ras pathway in lymphocytes of patients with CIU: possible mechanisms leading to autoimmune disease. Genetically determined aberrant p21Ras signaling interferes with thymic T-cell selection (1), leading to release of self-aggressive T cells (2). Alternatively, exposure to unknown environmental trigger (3) results in aberrant signaling in B and T cells (4) and disrupts immune balance. T-cell-assisted (5) production of anti-FcϵRI autoantibodies (Auto Ab's) by B cells (6) and direct interaction of autoimmune T cells with mast cells (7) lead to autoimmune chronic urticaria. GAP, Guanosine triphosphatase-activating protein; MAPK, mitogen-activated protein kinase. From Confino-Cohen R, Aharoni D, Goldberg A, Gurevitch I, Buchs A, Weiss M, et al. Evidence for aberrant regulation of the p21Ras pathway in PBMCs of patients with chronic idiopathic urticaria. J Allergy Clin Immunol 2002;109:349-56. Used with permission. Journal of Allergy and Clinical Immunology 2003 111, S805-S812DOI: (10.1067/mai.2003.155) Copyright © 2003 Mosby, Inc. Terms and Conditions