Anti-IgE receptor autoantibodies
The high-affinity IgE receptor (FceRl) exists on the surface of mast cells such as basophils. In 1989, Maront et al. Discovered that IgE mediated the formation of antigen-IgE-FceRI cross-linker on the cell surface, thereby activating mast cells and basophils, releasing histamine, leukotrienes and other substances. In 1991, Metzger et al. Reported that anti-IgE antibodies or anti-IgE receptor antibodies can also cross-link with IgE receptors, activating mast cells and basophils. IgE antibodies and FczRI antibodies were detected in the blood of patients with chronic urticaria (sustained release of histamine in serum). In 1995, Hidc et al reported that more than half of the patients with sustained release of histamine in this serum were FcaRI antibody positive.
1. Pathogenic effect After 30 minutes of intradermal injection of autologous serum, the subject's skin appeared wind clusters and flushing, which revealed the release of histamine in the serum and skin. This anti-autologous serum reaction gradually disappeared with the disappearance of clinical symptoms. Under the electron microscope, it was found that the mast cells at the skin test point had degranulation. Reveal the correlation between serum histamine releasing factor and allergic diseases.
2. Test method About half of the patients with positive skin test (Basophilic granulocyte release histidine test) are positive for anti-FctRIa or anti-IgE antibodies in the serum. The detection method of histamine release analysis using normal human basophils is more sensitive than the skin test method. This method is very sensitive to the detection of monoclonal anti-IgE receptor antibodies at small concentrations (approximately 3ng / m1). It does not require pretreatment of serum samples, but it is affected by the characteristics of basophils (especially they are sensitive to IgE Sex degree).
A study of monoclonal antibodies against IgE receptors revealed that they can bind FctRI competitively with IgE, and the binding site is located at the C-terminus of the extracellular region of FceRI. IgG-type antibodies obtained from the serum of patients with chronic urticaria were used to bind Chinese hamster cells (CHO) expressing human IgE receptors, and the bound IgG antibodies were detected by FctRI-coated ELISA method. The amount of bound IgG correlates well with basophilic histamine-releasing activity. The disadvantage of this method is that there is non-specific binding of IgG in some normal human serum. This binding is partially dependent on the cellular source of recombinant FctRI, and it also reflects the cross-reactivity between antibodies and non-human recombinant FctRI.
3. Clinical significance Chronic urticaria is characterized by recurrent skin wheals and flushing, which is caused by the release of allergic substances such as histamine due to the activation of skin mast cells by immune and / or non-immune factors. About 60% have a positive auto-sera skin test, and about 25% of patients have FcaRl2 autoantibodies. The ratio of men to women is 1:53.
About one-third of FcaRIa antibodies are competitive antibodies, which compete with IgE for binding to FcaRI. Contained in serum
The serum IgE concentration of patients with competitive FcaRI antibody decreased. In vitro experiments confirmed that FcaRIa antibody-positive serum in patients with chronic urticaria cannot induce basophils and skin mast cells to release histamine, which is derived from mast cells in the lung, heart and small intestine Degranulation, indicating that FcaRI antibody is involved in the pathogenesis of certain allergic and trans-diseases.
Many patients with chronic urticaria antagonize conventional antihistamine H1 receptors and even antihistamine H2 receptor drugs, which is quite effective for certain immunomodulatory treatments. Plasma exchange can temporarily relieve symptoms or achieve effective treatment. Intravenous injection of high doses of immunoglobulin can relieve the symptoms of patients who develop obvious skin reactions after injection of autologous serum. For patients with severe chronic urticaria, low-dose cyclosporin A can be used, but it will cause headaches and side effects (mainly relapse immediately after drug withdrawal). Some more specific treatments, such as immunoadsorption with IgE receptors or their analogs, are still under development.
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