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IgE plays a central role in the physiopathology of allergic rhinitis (AR).IgE-抗原免疫复合物对肥大细胞的结合触发其脱粒和炎症介质的释放，并与其他效应细胞（嗜酸性粒细胞，嗜碱性粒细胞）的募集。这是在我们经典发现高血清IgE水平的过敏性疾病治疗中使用抗IgE抗体的基础。Omalizumab is the first and best-known anti-IgE [1].It is a recombinant humanized IgG1 monoclonal antibody [2].它与IgE的Cε3结构域结合而不诱导肥大细胞和嗜碱性粒细胞脱粒（IgE通过其Cε3结构域与肥大细胞和嗜碱性粒细胞的FcεRI受体结合，从而导致脱粒化）[3]。This prevents IgE binding to effector cells, thereby inhibiting their stimulation.Through this mechanism of action, omalizumab reduces serum IgE levels and the number of FcεRI receptors [1].It also reduces IgE production by inhibiting allergen presentation [1].IgE-dependent activation and degranulation of mast cells and basophils is thus inhibited.
Singh P等。 PGPR介导的防御启动
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