𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Toll-like receptors in inflammatory bowel diseases: A decade later

✍ Scribed by Elke Cario


Publisher
John Wiley and Sons
Year
2010
Tongue
English
Weight
364 KB
Volume
16
Category
Article
ISSN
1078-0998

No coin nor oath required. For personal study only.

✦ Synopsis


Differential alteration of Toll-like receptor (TLR) expression in inflammatory bowel disease (IBD) was first described 10 years ago. Since then, studies from many groups have led to the current concept that TLRs represent key mediators of innate host defense in the intestine, involved in maintaining mucosal as well as commensal homeostasis. Recent findings in diverse murine models of colitis have helped to reveal the mechanistic importance of TLR dysfunction in IBD pathogenesis. It has become evident that environment, genetics, and host immunity form a multidimensional and highly interactive regulatory triad that controls TLR function in the intestinal mucosa. Imbalanced relationships within this triad may promote aberrant TLR signaling, critically contributing to acute and chronic intestinal inflammatory processes in IBD colitis and associated cancer.


πŸ“œ SIMILAR VOLUMES


Therapeutic impact of toll-like receptor
✍ Elke Cario πŸ“‚ Article πŸ“… 2008 πŸ› John Wiley and Sons 🌐 English βš– 438 KB

Recent studies have begun to define the mechanisms through which Toll-like receptors (TLRs) regulate intestinal homeostasis in health and disease. Current therapies for inflammatory bowel diseases (IBDs) mostly aim at interrupting the inflammatory cascade through agents that regulate TH1 or TH2 cyto

Systemic toll-like receptor ligands modi
✍ Marie McDonnell; YanMei Liang; Ansu Noronha; Jennifer Coukos; Dennis L. Kasper; πŸ“‚ Article πŸ“… 2011 πŸ› John Wiley and Sons 🌐 English βš– 901 KB

Background: Bacteria have a central, although poorly understood, role in inflammatory bowel disease (IBD). Host-bacteria interactions primarily take place in the gastrointestinal tract, but cells may also encounter translocated bacteria in the bloodstream. IBD is associated with activated, circulati

Toll-like receptor 4: A starting point f
✍ Anna Alisi; Nadia Panera; Valerio Nobili πŸ“‚ Article πŸ“… 2009 πŸ› John Wiley and Sons 🌐 English βš– 146 KB

2. Other local factors clearly existed, such as pancreatitis or splenectomy. 3. Cirrhosis was in a compensated condition. In reverse, PVT with well-compensated cirrhosis should not be excluded from noncirrhotic PVT. The effect can be better only if we aim at the major etiology more accurately and

Association of peroxisome proliferator-a
✍ Szilard Poliska; Andras Penyige; Peter Laszlo Lakatos;; the Hungarian IBD Study πŸ“‚ Article πŸ“… 2012 πŸ› John Wiley and Sons 🌐 English βš– 853 KB

Background: Inflammatory bowel disease (IBD) shows increasing incidence in the last few years in Eastern Europe, including Hungary. Since genetic susceptibility of patients plays an important role in the development and pathogenesis of IBD, it is important to identify new susceptibility genes. Perox