title: Involvement of Th1 cells and heat shock protein 60 in the pathogenesis of intestinal Behcet's disease.
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.
authors.affiliation: Department of Medicine, St Marianna University School of Medicine, Kawasaki, Kanagawa, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Imamura
authors.forename: M S
authors.initials: MS
authors.lastname: Kurokawa
authors.forename: H
authors.initials: H
authors.lastname: Yoshikawa
authors.forename: K
authors.initials: K
authors.lastname: Nara
authors.forename: E
authors.initials: E
authors.lastname: Takada
authors.forename: C
authors.initials: C
authors.lastname: Masuda
authors.forename: S
authors.initials: S
authors.lastname: Tsukikawa
authors.forename: S
authors.initials: S
authors.lastname: Ozaki
authors.forename: T
authors.initials: T
authors.lastname: Matsuda
authors.forename: N
authors.initials: N
authors.lastname: Suzuki
mesh_terms: D000328:Adult; D001528:Behcet Syndrome / Q000209:etiology* / Q000276:immunology; D016022:Case-Control Studies; D018834:Chaperonin 60 / Q000032:analysis* / Q000097:blood; D054407:Chemokine CCL4; D005260:Female; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007371:Interferon-gamma / Q000235:genetics; D018664:Interleukin-12 / Q000235:genetics; D015847:Interleukin-4 / Q000235:genetics; D007422:Intestines / Q000276:immunology*; D019402:Macrophage Inflammatory Proteins / Q000235:genetics; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis; D019713:Receptors, CCR5 / Q000235:genetics; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: C515187:CXCR3 protein, human; D018834:Chaperonin 60; D054407:Chemokine CCL4; D019402:Macrophage Inflammatory Proteins; D012333:RNA, Messenger; D019713:Receptors, CCR5; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma