Kimura Y, Pawankar R, Aoki M, Niimi Y, Kawana S
Department of Dermatology, Nippon Medical School, Tokyo, Japan.
Clin Exp Allergy. 2002 Dec;32(12):1787-93. doi: 10.1046/j.1365-2222.2002.01552.x.
Kimura's disease (KD) is a chronic inflammatory disorder characterized by tumours in the head and neck region, enlarged lymph nodes, increased eosinophil counts andhigh serum IgE. Mast cells are known to play a central role in IgE-mediated allergic diseases through the release of inflammatory mediators like IL-4, IL-5 and chemokines. We hypothesized that mast cells may play a role in the pathogenesis of KD by regulating eosinophilic infiltration and IgE synthesis.
In order to investigate the role of mast cells in the pathogenesis of KD, we examined the expression of cytokines/chemokines in the lesions of KD.
We examined the number of tryptase+ cells, EG2+ cells, CD3+ cells, IL-4+ cells, IL-5+ cells, eotaxin+ cells, RANTES+ cells and CCR3+ cells in five specimens of KD versus normal tissues by immunohistochemistry. The sources of IL-4, IL-5, eotaxin and RANTES and the expression of CCR3 were examined by immunostaining of serial sections with antibodies to IL-4, IL-5, eotaxin, RANTES and CCR3, and antibodies to tryptase, ECP (EG2) and CD3.
Mast cells, activated eosinophils, T cells, IL-4+ cells, IL-5+ cells, eotaxin+ cells, RANTES+ cells and CCR3+ cells were all increased in the lesions of KD as compared with those in normal tissue. Mast cells and T cells were the major source of IL-4, whereas mast cells, T cells and activated eosinophils were the main source of IL-5. Mast cells, T cells and activated eosinophils were the main source of eotaxin and RANTES.
The number of IL-4, IL-5, eotaxin and RANTES-expressing mast cells and T cells were increased in the lesions of KD. As mast cells are lesional resident cells, these cells may play an important role in the pathogenesis of KD by regulating IgE synthesis and orchestrating eosinophilic infiltration.
木村病（KD）是一种慢性炎症性疾病，其特征为头颈部肿瘤、淋巴结肿大、嗜酸性粒细胞计数增加及血清IgE升高。已知肥大细胞通过释放白细胞介素-4（IL-4）、白细胞介素-5（IL-5）和趋化因子等炎症介质在IgE介导的过敏性疾病中起核心作用。我们推测肥大细胞可能通过调节嗜酸性粒细胞浸润和IgE合成在KD的发病机制中发挥作用。
为了研究肥大细胞在KD发病机制中的作用，我们检测了KD病变中细胞因子/趋化因子的表达。
我们通过免疫组织化学检测了5例KD标本与正常组织中类胰蛋白酶+细胞、EG2+细胞、CD3+细胞、IL-4+细胞、IL-5+细胞、嗜酸性粒细胞趋化因子+细胞、调节激活正常T细胞表达和分泌的趋化因子（RANTES）+细胞及CC趋化因子受体3（CCR3）+细胞的数量。通过用抗IL-4、IL-5、嗜酸性粒细胞趋化因子、RANTES和CCR3的抗体以及抗类胰蛋白酶、嗜酸性粒细胞阳离子蛋白（EG2）和CD3的抗体对连续切片进行免疫染色，检测IL-4、IL-5、嗜酸性粒细胞趋化因子和RANTES的来源以及CCR3的表达。
与正常组织相比，KD病变中的肥大细胞、活化嗜酸性粒细胞、T细胞、IL-4+细胞、IL-5+细胞、嗜酸性粒细胞趋化因子+细胞、RANTES+细胞和CCR3+细胞均增多。肥大细胞和T细胞是IL-4的主要来源，而肥大细胞、T细胞和活化嗜酸性粒细胞是IL-5的主要来源。肥大细胞、T细胞和活化嗜酸性粒细胞是嗜酸性粒细胞趋化因子和RANTES的主要来源。
KD病变中表达IL-4、IL-5、嗜酸性粒细胞趋化因子和RANTES的肥大细胞和T细胞数量增加。由于肥大细胞是病变中的驻留细胞，这些细胞可能通过调节IgE合成和协调嗜酸性粒细胞浸润在KD的发病机制中发挥重要作用。
