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Toll-like receptors: the key to the stable door?
Severe sepsis continues to lead to critical illness. Few therapeutic options exist other than antibiotic therapy and general supportive care. Large numbers of patients continue to die as a consequence of overactivation of the host inflammatory response and the resultant coagulopathy and disregulatio...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2002
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC137300/ https://www.ncbi.nlm.nih.gov/pubmed/11983029 http://dx.doi.org/10.1186/cc1481 |
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author | Hopkins, Philip Cohen, Jonathan |
author_facet | Hopkins, Philip Cohen, Jonathan |
author_sort | Hopkins, Philip |
collection | PubMed |
description | Severe sepsis continues to lead to critical illness. Few therapeutic options exist other than antibiotic therapy and general supportive care. Large numbers of patients continue to die as a consequence of overactivation of the host inflammatory response and the resultant coagulopathy and disregulation of the normal controls of vasoactive tone. It is now known that a critical part of this host response occurs at the level of innate defence, without the need for antigen processing or the clonal expansion of cells targeted against the invading pathogen. This commentary will discuss the therapeutic targets revealed by our new understanding of the Toll-like receptor. The potential clinical difficulties that may result from intervention at this pattern-recognition receptor will also be explored. |
format | Text |
id | pubmed-137300 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-1373002003-02-27 Toll-like receptors: the key to the stable door? Hopkins, Philip Cohen, Jonathan Crit Care Commentary Severe sepsis continues to lead to critical illness. Few therapeutic options exist other than antibiotic therapy and general supportive care. Large numbers of patients continue to die as a consequence of overactivation of the host inflammatory response and the resultant coagulopathy and disregulation of the normal controls of vasoactive tone. It is now known that a critical part of this host response occurs at the level of innate defence, without the need for antigen processing or the clonal expansion of cells targeted against the invading pathogen. This commentary will discuss the therapeutic targets revealed by our new understanding of the Toll-like receptor. The potential clinical difficulties that may result from intervention at this pattern-recognition receptor will also be explored. BioMed Central 2002 2002-03-12 /pmc/articles/PMC137300/ /pubmed/11983029 http://dx.doi.org/10.1186/cc1481 Text en Copyright © 2002 BioMed Central Ltd |
spellingShingle | Commentary Hopkins, Philip Cohen, Jonathan Toll-like receptors: the key to the stable door? |
title | Toll-like receptors: the key to the stable door? |
title_full | Toll-like receptors: the key to the stable door? |
title_fullStr | Toll-like receptors: the key to the stable door? |
title_full_unstemmed | Toll-like receptors: the key to the stable door? |
title_short | Toll-like receptors: the key to the stable door? |
title_sort | toll-like receptors: the key to the stable door? |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC137300/ https://www.ncbi.nlm.nih.gov/pubmed/11983029 http://dx.doi.org/10.1186/cc1481 |
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