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 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.
Hopkins
Philip
P
Clinical Research Fellow, Department of Infectious Diseases, Hammersmith Hospital, London, UK. p.hopkins@ic.ac.uk
Cohen
Jonathan
J
D003422:Critical Care; D029721:Drosophila Proteins; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology* / Q000627:therapeutic use; D011956:Receptors, Cell Surface / Q000502:physiology* / Q000627:therapeutic use; D018805:Sepsis / Q000188:drug therapy / Q000191:economics / Q000401:mortality*; D051193:Toll-Like Receptors
D029721:Drosophila Proteins; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors