Cell Contact–Dependent Immunosuppression by Cd4+Cd25+Regulatory T Cells Is Mediated by Cell Surface–Bound Transforming Growth Factor β
- Kazuhiko Nakamura, A. Kitani, W. Strober
- BiologyJournal of Experimental Medicine
- 3 September 2001
It is demonstrated that CD4+CD25+ T cells do produce high levels of transforming growth factor (TGF)-β1 and interleukin (IL)-10 compared with CD4-CD25− T cells when stimulated by plate-bound anti- CD3 and soluble anti-CD28 and/or IL-2, and secretion of TGF-β1 (but not other cytokines), and it is observed here that such suppression is abolished by the presence of anti–
The immunological and genetic basis of inflammatory bowel disease
- G. Bouma, W. Strober
- Medicine, BiologyNature reviews. Immunology
- 1 July 2003
The most important finding is the identification of mutations in the gene that encodes NOD2 (nucleotide-binding oligomerization domain 2) protein in a subgroup of patients with Crohn's disease.
The immunology of mucosal models of inflammation.
- W. Strober, I. Fuss, R. Blumberg
- MedicineAnnual Review of Immunology
- 2002
This work analyzes the immunology of the IBDs through the lens of the murine models, first by drawing attention to their common features and then by considering individual models at a level of detail necessary to reveal their individual capacities to provide insight into IBD pathogenesis.
The fundamental basis of inflammatory bowel disease.
- W. Strober, I. Fuss, P. Mannon
- MedicineJournal of Clinical Investigation
- 1 March 2007
It is concluded that IBD is indeed characterized by an abnormal mucosal immune response but that microbial factors and epithelial cell abnormalities can facilitate this response.
Disparate CD4+ lamina propria (LP) lymphokine secretion profiles in inflammatory bowel disease. Crohn's disease LP cells manifest increased secretion of IFN-gamma, whereas ulcerative colitis LP cells…
- I. Fuss, M. Neurath, W. Strober
- Medicine, BiologyJournal of Immunology
- 1 August 1996
These studies provide strong evidence that the immunopathologic process characteristic of the two major forms of IBD is associated with very different cytokine secretion patterns, which may determine the type of inflammatory process present.
Proinflammatory cytokines in the pathogenesis of inflammatory bowel diseases.
- W. Strober, I. Fuss
- Biology, MedicineGastroenterology
- 1 May 2011
This review will explore the cytokine landscape with the view of providing an understanding of how recent and future anticytokine therapies actually function.
Trypan Blue Exclusion Test of Cell Viability
- W. Strober
- BiologyCurrent Protocols in Immunology
- 1 May 2001
The protocol described in this appendix allows for light microscopic quantitation of cell viability. Cells are suspended in PBS containing trypan blue and then examined to determine the percentage of…
Cutting Edge: Regulatory T Cells Induce CD4+CD25−Foxp3− T Cells or Are Self-Induced to Become Th17 Cells in the Absence of Exogenous TGF-β
- Lili Xu, A. Kitani, I. Fuss, W. Strober
- BiologyJournal of Immunology
- 1 June 2007
Results indicate that CD4+CD25+Foxp3+ regulatory T cells can function as inducers of Th 17 cells and can differentiate into Th17 cells, which have important implications to the understanding of regulatory T cell function and their possible therapeutic use.
Antibodies to interleukin 12 abrogate established experimental colitis in mice
- M. Neurath, I. Fuss, B. Kelsall, E. Stüber, W. Strober
- Biology, MedicineJournal of Experimental Medicine
- 1 November 1995
The data demonstrate the pivotal role of IL-12 and IFN-gamma in a TNBS-induced murine model of chronic intestinal inflammation and suggest the potential utility of anti-IL-12 antibodies in patients with Crohn's disease.
Interactions among the transcription factors Runx1, RORγt and Foxp3 regulate the differentiation of interleukin 17–producing T cells
- Fuping Zhang, Guangxun Meng, W. Strober
- BiologyNature Immunology
- 12 October 2008
The data support a model in which the differential association of Runx1 with Foxp3 and with RORγt regulates TH-17 differentiation, and suggest that optimal transcription of the gene encoding interleukin 17 required a 2-kilobase promoter and at least one conserved noncoding sequence, CNS-5.
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