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1

Immunotherapy of inflammatory bowel diseases: current concepts and future perspectives

100%
Neurath M. F.
Archivum Immunologiae et Therapiae Experimentalis
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2000
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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

The emerging distinct role of TNF-receptor 2 (p80) signaling in chronic inflammatory disorders

45%
Holtmann M. H., Schuchmann M., Zeller G., Galle P. R., Neurath M. F.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 4
279-287
EN
Tumor necrosis factor (TNF)-alpha is a pleiotropic cytokine with strong proinflammatory and immunomodulatory properties. TNF-alpha plays a critical role in many acute or chronic inflammatory diseases and anti-TNF strategies have proven to be clinically effective. Two TNF-specific cell surface receptors, TNF-R1 (p60) and TNF-R2 (p80), have been identified and the function of these receptors and the downstream intracellular signal-transduction pathways have been extensively studied in vitro. For a long time p60 was considered to be the predominant mediator of TNF signaling, whereas p80 was ascribed only an euxilliary function. However, there is increasing clinica and experimental evidence for an important independent role of p80 signaling in chronic inflammatory conditions. The date, most data exist for Crohn's disease. Upregulation of p80 and increased p80 signaling aggrevates experimental colitis and is likely to contribute to the chronicity of inflammation in vivo. Further studies are required to elucidate critically important steps in TNF signaling that might be dysregulated. This will lead to a better understanding of the pathogenesis of these diseases and poteintially reveal new, more specific therapeutic targets
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