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Th1细胞和热休克蛋白60在肠道白塞病发病机制中的作用。

Involvement of Th1 cells and heat shock protein 60 in the pathogenesis of intestinal Behcet's disease.

作者信息

Imamura Y, Kurokawa M S, Yoshikawa H, Nara K, Takada E, Masuda C, Tsukikawa S, Ozaki S, Matsuda T, Suzuki N

机构信息

Department of Medicine, St Marianna University School of Medicine, Kawasaki, Kanagawa, Japan.

出版信息

Clin Exp Immunol. 2005 Feb;139(2):371-8. doi: 10.1111/j.1365-2249.2005.02695.x.

Abstract

Involvement of excessive Th1 cell functions and heat shock protein expression in the pathogenesis of Behcet's disease (BD) has been reported. In this study we have characterized immune responses in intestinal lesions of BD. Peripheral blood lymphocytes (PBL) of BD and healthy controls (HC) and tissue specimens of intestinal Behcet's disease (intestinal BD), Crohn's disease (CD) and ulcerative colitis (UC) were analysed for mRNA and protein expression by reverse transcriptase-polymerase chain reaction (PCR) and immunohistochemistry, respectively. PBL of BD patients expressed the Th1-related chemokine receptor, CCR5 and CXCR3 preferentially compared with those of healthy controls. Intestinal lesions of BD expressed interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and interleukin (IL)-12 mRNA, indicating Th1 skewed responses in vivo. mRNA of Txk, a Tec family tyrosine kinase specific to Th1 cells, was expressed in the lesions, suggesting its contribution to the Th1-dominant responses. In the intestinal samples, CCR5 was detected in all the cases with BD, whereas Th2-related CCR3 and CCR4 were detected randomly, mainly in the cases with inactive BD and those receiving large amounts of prednisolone, indicating the Th1-dominant immune responses in the intestinal lesions. As the ligands of CCR5, MIP1alpha and MIP1beta were detected, whereas RANTES was not. Heat shock protein (HSP) 60 was expressed in PBL and intestinal tissues of BD. Th1-dominant immune responses and HSP60 expression may induce the inflammatory responses and thus be associated with the pathogenesis of intestinal BD.

摘要

已有报道称,过度的Th1细胞功能和热休克蛋白表达参与了白塞病(BD)的发病机制。在本研究中,我们对白塞病肠道病变中的免疫反应进行了特征分析。分别通过逆转录聚合酶链反应(PCR)和免疫组织化学分析了白塞病患者(BD)和健康对照者(HC)的外周血淋巴细胞(PBL)以及肠道白塞病(肠道BD)、克罗恩病(CD)和溃疡性结肠炎(UC)的组织标本的mRNA和蛋白表达。与健康对照者相比,BD患者的PBL优先表达Th1相关趋化因子受体CCR5和CXCR3。BD的肠道病变表达干扰素(IFN)-γ、肿瘤坏死因子(TNF)-α和白细胞介素(IL)-12 mRNA,表明体内存在Th1偏向性反应。Th1细胞特有的Tec家族酪氨酸激酶Txk的mRNA在病变中表达,提示其对Th1主导反应有贡献。在肠道样本中,所有BD病例均检测到CCR5,而Th2相关的CCR3和CCR4随机检测到,主要见于非活动期BD病例和接受大量泼尼松龙治疗的病例,表明肠道病变中存在Th1主导的免疫反应。作为CCR5的配体,检测到了MIP1α和MIP1β,而未检测到RANTES。热休克蛋白(HSP)60在BD患者的PBL和肠道组织中表达。Th1主导的免疫反应和HSP60表达可能诱导炎症反应,从而与肠道BD的发病机制相关。

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本文引用的文献

1
Infliximab maintenance therapy for fistulizing Crohn's disease.
N Engl J Med. 2004 Feb 26;350(9):876-85. doi: 10.1056/NEJMoa030815.
2
The role of heat shock proteins in Behçet's disease.
Clin Exp Rheumatol. 2003 Jul-Aug;21(4 Suppl 30):S44-8.
3
Biological therapy in Crohn's disease.
Hosp Med. 2003 Dec;64(12):708-12. doi: 10.12968/hosp.2003.64.12.2361.
4
Expression of CCR5 in Behçet's disease.
Adv Exp Med Biol. 2003;528:245-7. doi: 10.1007/0-306-48382-3_49.
5
T cells respond to heat shock protein 60 via TLR2: activation of adhesion and inhibition of chemokine receptors.
FASEB J. 2003 Aug;17(11):1567-9. doi: 10.1096/fj.02-1139fje. Epub 2003 Jun 17.
6
Human heat shock protein 60 induces maturation of dendritic cells versus a Th1-promoting phenotype.
J Immunol. 2003 Mar 1;170(5):2340-8. doi: 10.4049/jimmunol.170.5.2340.
8
Early up-regulation of chemokine expression in fulminant hepatic failure.
J Pathol. 2003 Mar;199(3):335-44. doi: 10.1002/path.1298.

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