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1
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0029127778
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Experimental models of inflammatory bowel disease
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Elson CO, Sartor RB, Tennyson GS, et al: Experimental models of inflammatory bowel disease. Gastroenterology 1995, 109:1344-1367. An excellent review of the many different types of inducible and spontaneous models of inflammatory bowel disease.
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(1995)
Gastroenterology
, vol.109
, pp. 1344-1367
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Elson, C.O.1
Sartor, R.B.2
Tennyson, G.S.3
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2
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0025899598
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Development and function of T cells in mice rendered interleukin-2 deficient by gene targeting
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Schorle H, Holtschke T, Hunig T, et al.: Development and function of T cells in mice rendered interleukin-2 deficient by gene targeting. Nature 1991, 352:621-624.
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(1991)
Nature
, vol.352
, pp. 621-624
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Schorle, H.1
Holtschke, T.2
Hunig, T.3
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3
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0027369395
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Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene
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Sadlack B, Merz H, Schorle H, et al.: Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene. Cell 1993, 75:253-261. One of the first papers to show that perturbations of the immune system could lead to tissue-damaging immune responses to the normal flora.
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(1993)
Cell
, vol.75
, pp. 253-261
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Sadlack, B.1
Merz, H.2
Schorle, H.3
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4
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0028783963
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Generalized autoimmune disease in interleukin-2-deficient mice is triggered by an uncontrolled activation and proliferation of CD4+ T cells
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Sadlack B, Lohler J, Schorle H, et al.: Generalized autoimmune disease in interleukin-2-deficient mice is triggered by an uncontrolled activation and proliferation of CD4+ T cells, Eur J Immunol 1995, 25:3053-3059. An interesting study showing that ona Balb/c background, IL-2 knockout mice develop general autoimmune disease.
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(1995)
Eur J Immunol
, vol.25
, pp. 3053-3059
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Sadlack, B.1
Lohler, J.2
Schorle, H.3
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5
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0030907897
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Characterisation of the mucosal cell-mediated immune response in IL-2 knockout mice before and after the onset of colitis
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McDonald SAC, Palmen MJHJ, Van Rees EP, et al.: Characterisation of the mucosal cell-mediated immune response in IL-2 knockout mice before and after the onset of colitis. Immunology 1997, 91:73-80 Polymerase chain reaction (PCR) was used to show that the gut lesion in IL-2 knockout mice develops prior to clinical disease and that the immune response in the mucosa has a Th1 cytokine profile. Also demonstrated upregulation of MAdCAM expression in inflamed bowel.
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(1997)
Immunology
, vol.91
, pp. 73-80
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McDonald, S.A.C.1
Palmen, M.J.H.J.2
Van Rees, E.P.3
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6
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0028877061
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T cells, but not B cells, are required for bowel inflammation in interleukin 2-deficient mice
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Ma A, Datta M, Margosian E, et al.: T cells, but not B cells, are required for bowel inflammation in interleukin 2-deficient mice. J Exp Med 1995, 182:1567-1572. Excellent simple paper showing that colitis in IL-2 knockout mice is T-cell-mediated.
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(1995)
J Exp Med
, vol.182
, pp. 1567-1572
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Ma, A.1
Datta, M.2
Margosian, E.3
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8
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0029609870
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Breakdown of tolerance to the intestinal bacterial flora in inflammatory bowel disease
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MacDonald TT: Breakdown of tolerance to the intestinal bacterial flora in inflammatory bowel disease. Clin Exp Immunol 1995, 102:445-447. An editorial summarizing much of the evidence implicating the normal flora in the pathogenesis of IBD in humans.
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(1995)
Clin Exp Immunol
, vol.102
, pp. 445-447
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MacDonald, T.T.1
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9
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0029586031
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Tolerance exists towards resident intestinal flora but is broken in active inflammatory bowel disease
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Duchmann R, Kaiser I, Hermann E, et al.: Tolerance exists towards resident intestinal flora but is broken in active inflammatory bowel disease. Clin Exp Immunol 1995, 102:448-455. An excellent paper showing that humans are immunologically tolerant to the antigens of the autologous flora, but respond to the antigens of the flora from other individuals. This tolerance is broken in IBD.
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(1995)
Clin Exp Immunol
, vol.102
, pp. 448-455
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Duchmann, R.1
Kaiser, I.2
Hermann, E.3
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10
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0028821858
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Immunopathology and interleukin (IL) 2-deficient mice: Thymus dependence and suppression by thymus-dependent cells with an intact IL-2 gene
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Kramer S, Schimpl A, Hunig T: Immunopathology and interleukin (IL) 2-deficient mice: thymus dependence and suppression by thymus-dependent cells with an intact IL-2 gene. J Exp Med 1995, 182:1769-1776.
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(1995)
J Exp Med
, vol.182
, pp. 1769-1776
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Kramer, S.1
Schimpl, A.2
Hunig, T.3
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12
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0027521572
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Interleukin-10 deficient mice develop chronic enterocolitis
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Kühn R, Löhler J, Rennick D, et al.: Interleukin-10 deficient mice develop chronic enterocolitis. Cell 1993, 75:263-274. Another of the first papers to show that disruption of an immunoregulatory cytokine allows tissue-damaging responses to the flora to develop in the gut.
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(1993)
Cell
, vol.75
, pp. 263-274
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Kühn, R.1
Löhler, J.2
Rennick, D.3
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13
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0029813545
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Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4+ Th1-like responses
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Berg DJ, Davidson N, Kuhn R, et al.: Enterocolitis and colon cancer in interleukin-10-deficient mice are associated with aberrant cytokine production and CD4+ Th1-like responses. J Clin Invest 1996, 98:1010-1020. An important study showing that the Th1-type cytokines are important in the tissue injury seen in IL-10 knockout mice.
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(1996)
J Clin Invest
, vol.98
, pp. 1010-1020
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Berg, D.J.1
Davidson, N.2
Kuhn, R.3
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14
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0030018186
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T helper cell 1-type CD4+ T cells, but not B cells, mediate colitis in interleukin 10-deficient mice
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Davidson NJ, Leach MW, Fort MM, et al.: T helper cell 1-type CD4+ T cells, but not B cells, mediate colitis in interleukin 10-deficient mice. J Exp Med 1996, 184:241-251. An important study showing that the enteropathy in IL-10 knockout mice is T-cell-mediated.
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(1996)
J Exp Med
, vol.184
, pp. 241-251
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Davidson, N.J.1
Leach, M.W.2
Fort, M.M.3
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15
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0027531528
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Transforming growth factor β1 null mutation in mice causes excessive inflammatory response and early death
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Kulkarni AB, Huh C-G, Becker D, et al: Transforming growth factor β1 null mutation in mice causes excessive inflammatory response and early death. Proc Natl Acad Sci USA 1993, 90:770-774.
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(1993)
Proc Natl Acad Sci USA
, vol.90
, pp. 770-774
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Kulkarni, A.B.1
Huh, C.-G.2
Becker, D.3
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16
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0029665856
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Critical role for β7 integrins in formation of the gut-associated lymphoid tissue
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Wagner N, Lohler l, Kunkel EJ, et al.: Critical role for β7 integrins in formation of the gut-associated lymphoid tissue. Nature 1996, 282:366-370. An excellent paper showing that β7 integrins are essential for the development of mucosal lymphoid tissue, presumably because lacking the a4β7 integrin, cells cannot migrate into the gut.
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(1996)
Nature
, vol.282
, pp. 366-370
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Wagner, N.1
Lohler, L.2
Kunkel, E.J.3
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17
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0030018413
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Defective Peyer's patch organogenesis in mice lacking the 55-kD receptor for tumor necrosis factor
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Neumann B, Luz A, Pfeffer K, et al.: Defective Peyer's patch organogenesis in mice lacking the 55-kD receptor for tumor necrosis factor. J Exp Med 1996, 184:259-264. Mice lacking the 55 kDa TNF receptor do not have Peyer's patches but have normal mucosal T-cells and B-cells. This calls into question the supposedly key role of Peyer's patches as the source of many of the T-and B-cells in the gut.
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(1996)
J Exp Med
, vol.184
, pp. 259-264
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Neumann, B.1
Luz, A.2
Pfeffer, K.3
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18
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0029866240
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high subset of CD4+ T cells
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high subset of CD4+ T cells. Am J Pathol 1996, 148:1503-1515. A very detailed histopathological study of the colitis seen in this model, emphasizing both the similarities and dissimilarities to Crohn's disease.
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(1996)
Am J Pathol
, vol.148
, pp. 1503-1515
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Leach, M.W.1
Bean, A.C.D.2
Mauze, S.3
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19
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0027517545
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Phenotypically different subsets of CD4+ T cells induce or protect from chronic inflammation in C.B-17 scid mice
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+ cells can cause colitis, presumably by responding to the flora, although this has not yet been formally demonstrated in this model.
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(1993)
Int Immunol
, vol.5
, pp. 1461-1471
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Powrie, F.1
Leach, M.W.2
Mauze, S.3
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20
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0028519015
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hi CD4+ T cells
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hi CD4+ T cells. Immunity 1994, 1:553-562. Colitis in this model can be inhibited by treating the mice with anti-TNF or anti-interferon-γ.
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(1994)
Immunity
, vol.1
, pp. 553-562
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Powrie, F.1
Leach, M.W.2
Mauze, S.3
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21
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0028033947
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Gut-homing CD4+ T cell receptor aβ+ T cells in the pathogenesis of murine inflammatory bowel disease
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+ cells when transferred in SCID mice cause colitis. The reasons for the differences between this paper and the work described in refs 18-20 are still unclear.
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(1994)
Eur J Immunol
, vol.24
, pp. 2803-2812
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Rudolphi, A.1
Boll, G.2
Poulsen, S.S.3
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22
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0029102210
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Severe colitis in mice with aberrant thymic selection
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Hollander CA, Simpson SJ, Mizoguchi E, et al.: Severe colitis in mice with aberrant thymic selection. Immunity 1995, 3:27-38. An as yet undefined alteration in the thymic environment of CD3ε transgenic mice means that T-cells educated in the thymus of these mice can cause colitis. The role of the flora in this model is not known.
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(1995)
Immunity
, vol.3
, pp. 27-38
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Hollander, C.A.1
Simpson, S.J.2
Mizoguchi, E.3
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23
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0029061801
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i2-deficient mice
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i2 gene in mice results in enhanced interferon-γ production by T-cells and colitis. It is assumed that these two events are related.
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(1995)
Nat Genet
, vol.10
, pp. 143-150
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Rudolph, U.1
Finegold, M.J.2
Rich, S.S.3
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24
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0027922467
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Spontaneous development of inflammatory bowel disease in T cell receptor mutant mice
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Mombaerts P, Mizoguchi E, Grusby MJ, et al: Spontaneous development of inflammatory bowel disease in T cell receptor mutant mice. Cell 1993, 75:275-282. This paper and ref 25 stand out from the rest in that it was unexpected that mice without αβ T-cells should develop colitis. These mice have major changes in their B-cell compartment. However, although it may seem counter-intuitive, they should be crossed onto Igμ knockouts to determine the exact role of B-cells in this system.
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(1993)
Cell
, vol.75
, pp. 275-282
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Mombaerts, P.1
Mizoguchi, E.2
Grusby, M.J.3
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25
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0029975876
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Cytokine imbalance and autoantibody production in T cell receptor-α mutant mice with inflammatory bowel disease
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+ TcR α-β+ T-cells producing interferon-γ in the inflamed colon.
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(1996)
J Exp Med
, vol.183
, pp. 847-856
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Mizoguchi, A.1
Mizoguchi, E.2
Chiba, C.3
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26
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0031012926
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T cell receptor-αβ deficient mice fail to develop colitis in the absence of a microbial flora
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Dianda L, Hanby A, Wright NA, et al.: T cell receptor-αβ deficient mice fail to develop colitis in the absence of a microbial flora. Am J Pathol 1997, 150:91-97. This paper shows that TcRα knockout mice do not develop colitis when made germ-free, nor when associated with a limited bacterial flora of Escherichia coli, Lactobacillus plantarum, Streptococcus faecalis and S. faecium.
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(1997)
Am J Pathol
, vol.150
, pp. 91-97
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Dianda, L.1
Hanby, A.2
Wright, N.A.3
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27
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10244252625
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Gastric mucosa abnormalities and tumorigenesis in mice lacking the pS2 trefoil protein
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Lefebvre O, Chenard M-P, Masson R, et al.: Gastric mucosa abnormalities and tumorigenesis in mice lacking the pS2 trefoil protein. Science 1996, 274:259-262. Mice lacking pS2 develop gastric cancer suggesting that pS2 functions as a tumour suppressor protein.
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(1996)
Science
, vol.274
, pp. 259-262
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Lefebvre, O.1
Chenard, M.-P.2
Masson, R.3
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28
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0029877816
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Transgenic mice that overexpress the human trefoil peptide pS2 have an increased resistance to intestinal damage
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Playford RJ, Marchbank T, Goodlad RA, et al.: Transgenic mice that overexpress the human trefoil peptide pS2 have an increased resistance to intestinal damage. Proc Natl Acad Sci USA 1996, 93:2137-2142. Beautiful study to show that enhancement of endogenous healing mechanisms using genetic manipulation makes the gut more resistant to injury.
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(1996)
Proc Natl Acad Sci USA
, vol.93
, pp. 2137-2142
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Playford, R.J.1
Marchbank, T.2
Goodlad, R.A.3
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29
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0029828745
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Impaired defense of intestinal mucosa in mice lacking intestinal trefoil factor
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Mashimo H, Wu D-C, Podolsky DK, et al.: Impaired defense of intestinal mucosa in mice lacking intestinal trefoil factor. Science 1996, 274:262-265. Another beautiful study showing that in the absence of intestinal trefoil factor, mucosal regeneration is impaired.
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(1996)
Science
, vol.274
, pp. 262-265
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Mashimo, H.1
Wu, D.-C.2
Podolsky, D.K.3
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30
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0028010074
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Immune mechanisms in chronic inflammatory bowel disease
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Braegger CP, MacDonald TT: Immune mechanisms in chronic inflammatory bowel disease. Ann Allergy 1994, 72:135-141.
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(1994)
Ann Allergy
, vol.72
, pp. 135-141
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Braegger, C.P.1
MacDonald, T.T.2
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31
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0027292917
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T cell activation can induce either mucosal destruction or adaptation in cultured human fetal small intestine
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Lionetti P, Breese E, Braegger CP, et al.: T cell activation can induce either mucosal destruction or adaptation in cultured human fetal small intestine. Gastroenterology 1993, 105:373-381.
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(1993)
Gastroenterology
, vol.105
, pp. 373-381
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Lionetti, P.1
Breese, E.2
Braegger, C.P.3
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32
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0031568392
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A major role for matrix metalloproteinases in T cell injury in the gut
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Pender SL-F, Docherty AJP, Tickle SP, et al: A major role for matrix metalloproteinases in T cell injury in the gut. J Immunol 1997, 158:1582-1590. Using expiant cultures of human fetal intestine it was demonstrated that a major component of injury mediated by Th1 responses in the gut is due to cytokine-activation of mucosal stromal cells to secrete tissue-degrading enzymes, notably stromelysin-1.
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(1997)
J Immunol
, vol.158
, pp. 1582-1590
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Pender, S.L.-F.1
Docherty, A.J.P.2
Tickle, S.P.3
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33
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9544226450
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Normal luminal bacteria, especially Bacteroides species, mediate chronic colitis, gastritis and arthritis in HLA-B27/human β2 microglobulin transgenic rats
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Rath HC, Herfarth HH, Ikeda JS, et al.: Normal luminal bacteria, especially Bacteroides species, mediate chronic colitis, gastritis and arthritis in HLA-B27/human β2 microglobulin transgenic rats. J Clin Invest 1996, 98:945-953. A landmark study showing directly that the normal flora can cause colitis and highlighting the fact that not all bacteria are equivalent in this activity.
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(1996)
J Clin Invest
, vol.98
, pp. 945-953
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Rath, H.C.1
Herfarth, H.H.2
Ikeda, J.S.3
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34
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0028972499
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Inflammatory bowel disease and adenomas in mice expressing a dominant negative N-cadherin
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Hermiston ML, Cordon JI: Inflammatory bowel disease and adenomas in mice expressing a dominant negative N-cadherin. Science 1995, 270:1203-1207. Probably the most important paper to be published in gastroenterology in recent years. Shows that disruption of the epithelial barrier by tissue-specific gene-targeting results in patchy transmural inflammation.
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(1995)
Science
, vol.270
, pp. 1203-1207
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Hermiston, M.L.1
Cordon, J.I.2
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