
pmid: 20039306
AbstractThere is almost no aspect of the immune response that is not regulated by TLR. Initially described as drivers of the innate immune response to pathogens, it is now clear that the TLR family can also influence most aspects of adaptive immunity, as well as determine how tissue cells interact with microbes in their environment. In particular, the intestine and its immune system must co‐exist with an enormous community of commensal bacteria and are also on constant alert against invading pathogens. Unsurprisingly, there is therefore great interest in how TLR might regulate physiological and pathological reactions in the gut. An article in this issue of the European Journal of Immunology addresses this question with some elegant experiments that indicate that TLR2 is not essential for the pathogenesis or T‐cell‐mediated regulation of different models of inflammatory bowel disease in mice.
Mice, Knockout, Forkhead Transcription Factors, Inflammatory Bowel Diseases, T-Lymphocytes, Regulatory, Toll-Like Receptor 2, Helicobacter Infections, Mice, Acute Disease, Chronic Disease, Host-Pathogen Interactions, Animals, Helicobacter hepaticus, Signal Transduction
Mice, Knockout, Forkhead Transcription Factors, Inflammatory Bowel Diseases, T-Lymphocytes, Regulatory, Toll-Like Receptor 2, Helicobacter Infections, Mice, Acute Disease, Chronic Disease, Host-Pathogen Interactions, Animals, Helicobacter hepaticus, Signal Transduction
| citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 14 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Average | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Average | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
