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1

Immunotherapy of inflammatory bowel diseases: current concepts and future perspectives

100%
Neurath M. F.
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vol. 48
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issue 2
81-84
EN
The etiology and the pathogenesis of inflammatory bowel diseases (IBD), e. g. Crohn's disease and ulcerative colitis are still not completely understood. However, there is growing evidence that an alteration of the mucosal immune system towards luminal antigens in a genetically susceptible host plays a key role in the pathogenesis of IBD. In particular, cytokines produced by intestinal epithelial cells, lamina propria macrophages and CD4+ T cells appear to contribute to the initiation and perpetuation of intestinal inflammation in IBD. This review focuses on the role of the mucosal immune system in the pathogenesis of IBD and potential novel immunotherapeutic strategies for chronic intestinal inflammation. Such strategies include recombinant antiinflammatory cytokines, neutralizing antibodies or fusion proteins, antisense oligonucleotides and adenoviral gene transfer.
2

Abnormalities in the handling of intracellular bacteria in Crohn's disease: a link between infectious etiology and host genetic susceptibility

100%
Glasser A.-L., Darfeuille-Michaud A.
Archivum Immunologiae et Therapiae Experimentalis
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2008
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vol. 56
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issue 4
237-244
EN
The etiology of Crohn's disease (CD) is still poorly understood, but recent advances have highlighted the importance of the innate immune system and the critical relationship between the gut flora and the intestinal mucosa. Several combinations of genetic factors predisposing to CD have been described, with the most significant replicable associations including genes for intracellular receptors of bacterial cell walls (NOD2/CARD15) and for bacterial clearance and antigen processing via autophagy (ATG16L1 and IRGM). One theoretical link between susceptibility genes NOD2/CARD15, ATG16L1, and IRGM is that CD is primarily induced by the presence of a dysfunctional immunological response to persistent infection by intracellular bacterial pathogens such as Mycobacterium avium subspecies paratuberculosis or adherent-invasive Escherichia coli, both first-rank candidates on the basis of host genetic susceptibility, which concerns impaired functions in the defense against intracellular bacteria.
3

Anti-apoptosis function of TNF-alpha in chronic lymphocytic leukemia: lessons from Crohn 's disease and the therapeutic potential of bupropion to lower TNF-alpha

86%
Kast R. E., Altschuler E. L.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 2
143-147
EN
Crohn's disease and B cell chronic lymphocytic leukemia (CLL) share a common link in their pathologic mechanisms. Lymphocytes in both diseases fail to undergo apoptosis and die properly. That failure is partly due to increased signaling by tumor necrosis factor (TNF)-alpha, and their respective pathologies directly follow from this apoptosis failure. Bupropion is a commonly used generic antidepressant in clinical use for over a decade, and early evidence indicates it lowers TNF levels. This paper suggests the use of bupropion in CLL to lower TNF levels, which may thereby slow CLL disease course.
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