Distribution and phenotype of Epstein-Barr virus-infected cells in inflammatory bowel disease

被引:68
作者
Spieker, T
Herbst, H
机构
[1] Free Univ Berlin, Klinikum Benjamin Franklin, Inst Pathol, D-12200 Berlin, Germany
[2] Goethe Univ Frankfurt, Senckenberg Ctr Pathol, D-6000 Frankfurt, Germany
[3] Univ Hosp Eppendorf, Inst Pathol, Hamburg, Germany
关键词
D O I
10.1016/S0002-9440(10)64516-6
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Little is known about Epstein-Barr virus (EBV) infection of colon mucosa, particularly in inflammatory bowel diseases. Crohn's disease acid ulcerative colitis are thought to differ in T-helper lymphocyte composition and cytokine secretion patterns. Some of the implicated cytokines are growth factors for EBV-infected cells. We examined colon mucosa for differences In the distribution and phenotype of EBV-infected cells. Colon tissues with Crohn's disease (n = 31) or ulcerative colitis (n = 25) and controls (n = 60) were characterized by in situ hybridization and immnohistology for six EBV gene products as indicators of latent and replicative EBV infection. The cells were additionally phenotyped by combined detection of the EBV transcripts and B- or T-cell antigens. B lymphocytes predominated as the site of latent EBV infection in the colon and were most numerous in ulcerative colitis. In active ulcerative colitis, EBV-positive lymphocytes accumulated under and within the epithelium and displayed evidence for replicative infection. The patterns of mucosal EBV gene expression indicate local impairment of virus-specific T-cell responses in active ulcerative colitis. Detection of EBV may help to discriminate between active ulcerative colitis and other inflammatory bowel diseases. Colon mucosa is a potential site of EBV replication and may be relevant for EBV transmission.
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页码:51 / 57
页数:7
相关论文
共 38 条
[1]   MORPHOLOGY, IMMUNOPHENOTYPE, AND DISTRIBUTION OF LATENTLY AND/OR PRODUCTIVELY EPSTEIN-BARR VIRUS-INFECTED CELLS IN ACUTE INFECTIOUS-MONONUCLEOSIS - IMPLICATIONS FOR THE INTERINDIVIDUAL INFECTION ROUTE OF EPSTEIN-BARR-VIRUS [J].
ANAGNOSTOPOULOS, I ;
HUMMEL, M ;
KRESCHEL, C ;
STEIN, H .
BLOOD, 1995, 85 (03) :744-750
[2]  
BAUMANN MA, 1992, BLOOD, V79, P1763
[3]   EPSTEIN-BARR-VIRUS TRANSFORMATION INDUCES LYMPHOCYTES-B TO PRODUCE HUMAN INTERLEUKIN-10 [J].
BURDIN, N ;
PERONNE, C ;
BANCHEREAU, J ;
ROUSSET, F .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 177 (02) :295-304
[4]   An interleukin 12-related cytokine is up-regulated in ulcerative colitis but not in Crohn's disease [J].
Christ, AD ;
Stevens, AC ;
Koeppen, H ;
Walsh, S ;
Omata, F ;
Devergne, O ;
Birkenbach, M ;
Blumberg, RS .
GASTROENTEROLOGY, 1998, 115 (02) :307-313
[5]   A T(H)1-]T(H)2 SWITCH IS A CRITICAL STEP IN THE ETIOLOGY OF HIV-INFECTION [J].
CLERICI, M ;
SHEARER, GM .
IMMUNOLOGY TODAY, 1993, 14 (03) :107-110
[6]  
CRADDOCK JM, 1970, APPL STAT, V19, P173
[7]  
DEAMANT FD, 1993, MODERN PATHOL, V6, P729
[8]   CD30, TH2 CYTOKINES AND HIV-INFECTION - A COMPLEX AND FASCINATING LINK [J].
DELPRETE, G ;
MAGGI, E ;
PIZZOLO, G ;
ROMAGNANI, S .
IMMUNOLOGY TODAY, 1995, 16 (02) :76-80
[9]   Distinct cytokine patterns in early and chronic ileal lesions of Crohn's disease [J].
Desreumaux, P ;
Brandt, E ;
Gambiez, L ;
Emilie, D ;
Geboes, K ;
Klein, O ;
Ectors, N ;
Cortot, A ;
Capron, M ;
Colombel, JF .
GASTROENTEROLOGY, 1997, 113 (01) :118-126
[10]  
FIORENTINO DF, 1991, J IMMUNOL, V146, P3444