RESUMO
A large number of studies have shown that immunoglobulin E (IgE) not only participates in the occurrence and development of allergic reactions, but also induces and aggravates autoimmune reactions through various mechanisms. IgE autoantibodies have been confirmed to be present in a variety of autoimmune skin diseases, and may be involved in the occurrence and development of related diseases by affecting multiple immune cells such as dendritic cells, mast cells, and basophils via binding to autoantigens. This review summarizes the role and possible mechanism of action of IgE in the induction and exacerbation of autoimmune skin diseases such as systemic lupus erythematosus, bullous pemphigoid and chronic idiopathic urticaria, and provides a theoretical basis for clinical diagnosis and treatment.
RESUMO
IgE is closely related to autoimmune diseases.On the one hand,a variety of autoimmune diseases found the increasing IgE.This IgE is just as allergen-specific IgE or IgE autoantibody is not yet clear.On the other hand, the pathogenic mechanism of IgE includes not only the direct damage due to immune complex deposition,activation of basophils and mast cells releasing inflammatory mediators,but also includes the autoimmune effects of type I interferons produced by plasma cell -like dendritic cells.This article expounds the relationship between IgE and the occurrence and development of several autoimmune diseases.
RESUMO
Background: Chronic urticaria patients who demonstrate autoantibodies against the high-affinity receptor of IgE (FceRI) or IgE itself tend to have a high itch and wheal score, and systemic symptoms may have a significant bearing on their management in terms of super pharmacologic doses of antihistamines needed or use of immunomodulators. Most studies have used histamine release assays rather than autologous serum skin tests (ASSTs) for correlating urticaria severity and histamine releasing activity. Methods: An ASST was performed in 100 (M:F, 31:69) chronic urticaria patients aged between 14 and 63 (mean, 32.69 ± 13) years with an objective to study the clinicoepidemiologic features like age, sex, age of onset and duration, frequency and distribution of wheals, urticaria severity, angioedema and systemic manifestations in ASST-positive and ASST-negative patients. Results: ASST was positive in 46% of the patients and negative in 54% of the patients, respectively. Both groups showed no statistically significant difference for epidemiological details. However, the ASST-positive patients had a higher mean urticaria activity score, frequent involvement of more body sites, particularly palms and soles, presence of throat angioedema and general constitutional, respiratory or gastrointestinal symptoms in comparison with the ASST-negative patients. Conclusions: Apparently, ASST-positive patients have more severe clinical manifestations of chronic urticaria. The knowledge will be useful for the treating dermatologists and patients alike in view of its therapeutic implications.