嗜酸性粒细胞增生性淋巴肉芽肿的免疫研究进展

Eosinophilic hyperplastic lymphogranuloma, is also known as Kimura’s disease(KD), causes elevated eosinophils and serum IgE. The low-affinity IgE receptor is expressed on the surface of B and T cells, as well as eosinophils, and regulates various immune responses. Increased IgG4 is deemed a benign antibody without pathogenicity in primary and recurrent KD. Provision of chemokines, adhesion molecules, and trophic factors induce follicular dendritic cells to participate in the shaping of B cell responses and molding of the local microenvironment. Eosinophil cationic protein from eosinophils is an important agent in KD mechanism. The hyper-responsiveness of C5a in KD plasma may be important in regulating cellular response after complementary activation. Interleukin(IL)-4 induces IgE synthesis. IL-5, granulocyte macrophage colony-stimulating factor, and IL-3 lead to focal eosinophil infiltration. Eotaxin and regulated upon activation normal T cell expressed and secreted factor would also help to boost eosinophils concentration in inflammation. T helper(T_h) cells are subdivided into the T_h1 and T_h2 subsets. T_h1 cells are primarily involved in cellmediated immune responses, whereas T_h2 cells fulfill an important role in humoral and allergic immune responses. Lifted eosinophils and serum IgE may be caused by T_h2 polarization in the KD mechanism.