Inter J Stomatol ›› 2016, Vol. 43 ›› Issue (2): 181-186.doi: 10.7518/gjkq.2016.02.015

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Research progress on the immunity of eosinophilic hyperplastic lymphogranuloma

Chen Qingli, Srijana Dwa, Karmesh Bajracharya, Gong Zhongcheng   

  1. Dept. of Maxillofacial Tumor Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, China)
  • Received:2015-09-15 Revised:2015-12-08 Online:2016-03-01 Published:2016-03-01

Abstract: 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(Th) cells are subdivided into the Th1 and Th2 subsets. Th1 cells are primarily involved in cellmediated immune responses, whereas Th2 cells fulfill an important role in humoral and allergic immune responses. Lifted eosinophils and serum IgE may be caused by Th2 polarization in the KD mechanism.

Key words: eosinophilic hyperplastic lymphogranuloma, Kimura’s disease, immunologic derangement, eosinophilic hyperplastic lymphogranuloma, Kimura’s disease, immunologic derangement

CLC Number: 

  • Q 256

TrendMD: 
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