T-cell transfer and cytokine/TCR gene deletion models in the study of inflammatory bowel disease

被引:19
作者
Bregenholt, S
Delbro, D
Claesson, MH
机构
[1] UNIV COPENHAGEN, PANUM INST, DEPT MED ANAT, DK-2200 COPENHAGEN N, DENMARK
[2] GOTHENBURG UNIV, SAHLGRENSKA SJUKHUSET, DEPT SURG, S-41124 GOTHENBURG, SWEDEN
关键词
inflammatory bowel disease; T cells; cytokines; immunoglobulins; scid mice;
D O I
10.1111/j.1699-0463.1997.tb05068.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Until recently there existed no appropriate immunological animal models for human inflammatory bowel diseases (IBD). Today a number of models, mostly in the mouse and rat, have proved useful in the study of several aspects of IBD, including the histopathology and the disease-inductive and -protective cell types, subsets and cytokines, for example CD4(+) T cells, IFN gamma, IL-12, IL-2, IL-10 and TGF beta. Furthermore, these recent IBD models make it possible to examine various chemo-and immunotherapeutic approaches. This review focuses on IBD development in adoptive T-cell transfer models and in gene-deleted mice.
引用
收藏
页码:655 / 662
页数:8
相关论文
共 40 条
[21]   CD4+ T-CELLS THAT EXPRESS HIGH-LEVELS OF CD45RB INDUCE WASTING DISEASE WHEN TRANSFERRED INTO CONGENIC SEVERE COMBINED IMMUNODEFICIENT MICE - DISEASE DEVELOPMENT IS PREVENTED BY COTRANSFER OF PURIFIED CD4+ T-CELLS [J].
MORRISSEY, PJ ;
CHARRIER, K ;
BRADDY, S ;
LIGGITT, D ;
WATSON, JD .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (01) :237-244
[22]   INCIDENCE AND PREVALENCE OF CROHNS-DISEASE IN THE COUNTY OF COPENHAGEN, 1962-87 - A SIXFOLD INCREASE IN INCIDENCE [J].
MUNKHOLM, P ;
LANGHOLZ, E ;
NIELSEN, OH ;
KREINER, S ;
BINDER, V .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1992, 27 (07) :609-614
[23]   INFLAMMATORY BOWEL-DISEASE .2. [J].
PODOLSKY, DK .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (14) :1008-1016
[24]   INFLAMMATORY BOWEL-DISEASE .1. [J].
PODOLSKY, DK .
NEW ENGLAND JOURNAL OF MEDICINE, 1991, 325 (13) :928-937
[25]   INHIBITION OF TH1 RESPONSES PREVENTS INFLAMMATORY BOWEL-DISEASE IN SCID MICE RECONSTITUTED WITH CD45RB(HI) CD4(+) T-CELLS [J].
POWRIE, F ;
LEACH, MW ;
MAUZE, S ;
MENON, S ;
CADDLE, LB ;
COFFMAN, RL .
IMMUNITY, 1994, 1 (07) :553-562
[26]   A critical role for transforming growth factor-beta but not interleukin 4 in the suppression of T helper type 1-mediated colitis by CD45RB(low) CD4(+) T cells [J].
Powrie, F ;
Carlino, J ;
Leach, MW ;
Mauze, S ;
Coffman, RL .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (06) :2669-2674
[27]   PHENOTYPICALLY DISTINCT SUBSETS OF CD4(+) T-CELLS INDUCE OR PROTECT FROM CHRONIC INTESTINAL INFLAMMATION IN C - B-17 SCID MICE [J].
POWRIE, F ;
LEACH, MW ;
MAUZE, S ;
CADDLE, LB ;
COFFMAN, RL .
INTERNATIONAL IMMUNOLOGY, 1993, 5 (11) :1461-1471
[28]   A GUT-HOMING, OLIGOCLONAL CD4+ T-CELL POPULATION IN SEVERE-COMBINED IMMUNODEFICIENT MICE EXPRESSING A REARRANGED, TRANSGENIC CLASS I-RESTRICTED ALPHA-BETA-T-CELL RECEPTOR [J].
REIMANN, J ;
RUDOLPHI, A ;
SPIESS, S ;
CLAESSON, MH .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1995, 25 (06) :1643-1653
[29]   CD3+ T-CELLS IN SEVERE COMBINED IMMUNODEFICIENCY (SCID) MICE .3. TRANSFERRED CONGENIC, SELFREACTIVE CD4+ T-CELL CLONES RESCUE IGM-PRODUCING, SCID-DERIVED B-CELLS [J].
REIMANN, J ;
RUDOLPHI, A ;
CLAESSON, MH .
INTERNATIONAL IMMUNOLOGY, 1991, 3 (07) :657-663
[30]   SELECTIVE RECONSTITUTION OF LYMPHOCYTE-T SUBSETS IN SCID MICE [J].
REIMANN, J ;
RUDOLPHI, A ;
CLAESSON, MH .
IMMUNOLOGICAL REVIEWS, 1991, 124 :75-95