论文部分内容阅读
嗜酸性粒细胞增生性淋巴肉芽肿也称木村病(KD),伴有嗜酸性粒细胞和血清免疫球蛋白(Ig)E升高。低亲和力Ig E受体表达于B细胞、T细胞、嗜酸性粒细胞表面,调节各种免疫应答。在KD初发和复发患者中,Ig G4均增高,被看作非主要致病性抗体。滤泡树突细胞分泌的趋化因子、黏附分子和营养因子可调控B细胞免疫应答并作用于局部微环境。嗜酸性粒细胞分泌的嗜酸性粒细胞阳离子蛋白在KD发病过程中起着重要的作用。肥大细胞可促进嗜酸性粒细胞的浸润并诱导B细胞合成Ig E。KD患者血清补体C5a高反应性可以调节补体活化后介导的细胞免疫应答。白细胞介素(IL)-4可诱导Ig E合成,IL-5、粒细胞-巨噬细胞集落刺激因子和IL-3可促使嗜酸性粒细胞局灶浸润。嗜酸性粒细胞趋化因子与调节正常T细胞表达和分泌因子一起参与嗜酸性粒细胞在炎症处的聚集。Th细胞又分为Th1和Th2细胞,Th1细胞参与细胞免疫反应,Th2细胞参与体液免疫及变态反应性免疫反应。嗜酸性粒细胞增多及Ig E升高,可能系Th2细胞在KD发病机制中起着重要的作用。
Eosinophilic lymphogranuloma, also known as Kimura disease (KD), is associated with elevated eosinophils and serum immunoglobulin (Ig) E. Low affinity Ig E receptors are expressed on the surface of B cells, T cells and eosinophils and regulate various immune responses. Ig G4 is elevated in patients with primary and recurrent KD and is considered as a non-primary pathogenic antibody. Follicular dendritic cells secrete chemokines, adhesion molecules and trophic factors that regulate B-cell immune responses and act on the local microenvironment. Eosinophil secreted eosinophil cationic protein plays an important role in the pathogenesis of KD. Mast cells can promote eosinophil infiltration and induce B cells to synthesize IgE. Serum complement C5a hyperresponsiveness in KD patients can modulate the cellular immune response mediated by complement activation. IL-4 induces IgE synthesis, and IL-5, granulocyte-macrophage colony-stimulating factor and IL-3 promote eosinophilic focal infiltration. Eotaxin, along with regulation of normal T cell expression and secretion factors, is involved in the aggregation of eosinophils at the site of inflammation. Th cells are divided into Th1 and Th2 cells, Th1 cells are involved in cellular immune responses, and Th2 cells are involved in humoral and allergic immune responses. Eosinophilia and elevated IgE may be Th2 cells play an important role in the pathogenesis of KD.