Marone G, Spadaro G, Palumbo C, Condorelli G
Division of Clinical Immunology and Allergy, University of Naples Federico II School of Medicine, Italy.
Clin Exp Allergy. 1999 Jan;29(1):17-27. doi: 10.1046/j.1365-2222.1999.00441.x.
Basophil granulocytes and tissue mast cells and their mediators play a role in the pathogenesis of several immune and inflammatory disorders. Human basophils and mast cells (FcepsilonRI+ cells) can be activated through immunological interaction with the IgE-FcepsilonRI network. FcepsilonRI+ cells can be triggered by cross-linking between the Fab portions of IgE and multivalent antigens (direct anaphylaxis). 'Reverse type' anaphylaxis can occur through three distinct mechanisms: antibodies against the Fcepsilon portion of IgE (anti-IgE), antibodies against epitopes of the alpha chain of FcepsilonRI (anti-FcepsilonRIalpha) and anti-IgG acting on IgG-IgE complexes bound to FcepsilonRI. Anti-IgE autoantibodies are occasionally present even in normal donors and more frequently in a variety of allergic (chronic urticaria, atopic dermatitis and bronchial asthma) and autoimmune disorders (rheumatoid arthritis, lupus erythematosus and systemic sclerosis). IgG anti-IgE from a small percentage of patients induces the release of mediators from human FcepsilonRI+ cells. Some of the anti-IgE autoantibodies present in allergic patients are non-anaphylactogenic, thus representing a possible protective mechanism preventing the association of IgE with FcepsilonRI. Anti-FcepsilonRIalpha autoantibodies also occur in a significant percentage of patients of chronic urticaria and probably non-allergic asthma and some autoimmune diseases. Although anti-IgE and anti-FcepsilonRIalpha autoantibodies, present in a percentage of patients with immune disorders, are relevant to the pathogenesis of these conditions, much remains to be learnt about their immunochemistry, their prevalence and precise role in various inflammatory diseases.
嗜碱性粒细胞、组织肥大细胞及其介质在多种免疫和炎症性疾病的发病机制中起作用。人类嗜碱性粒细胞和肥大细胞（FcepsilonRI+细胞）可通过与IgE-FcepsilonRI网络的免疫相互作用而被激活。FcepsilonRI+细胞可由IgE的Fab段与多价抗原交联触发（直接过敏反应）。“反向型”过敏反应可通过三种不同机制发生：针对IgE的Fcepsilon部分的抗体（抗IgE）、针对FcepsilonRIα链表位的抗体（抗FcepsilonRIα）以及作用于与FcepsilonRI结合的IgG-IgE复合物的抗IgG。抗IgE自身抗体甚至偶尔在正常供体中出现，在各种过敏性疾病（慢性荨麻疹、特应性皮炎和支气管哮喘）和自身免疫性疾病（类风湿关节炎、红斑狼疮和系统性硬化症）中更常见。一小部分患者的IgG抗IgE可诱导人类FcepsilonRI+细胞释放介质。过敏性患者中存在的一些抗IgE自身抗体无过敏反应性，因此可能是一种防止IgE与FcepsilonRI结合的保护机制。抗FcepsilonRIα自身抗体也在相当比例的慢性荨麻疹患者以及可能的非过敏性哮喘患者和一些自身免疫性疾病患者中出现。尽管在一定比例的免疫疾病患者中存在的抗IgE和抗FcepsilonRIα自身抗体与这些疾病的发病机制有关，但关于它们的免疫化学、患病率及其在各种炎症性疾病中的精确作用仍有许多有待了解。
