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SUMMARY:Milstein Lecture 2012: How do we sense microbes?  From LPS\, TNF\,
  and the TLRs. - Bruce Beutler\, UT Southwestern Medical Centre
DTSTART:20120517T151500Z
DTEND:20120517T170000Z
UID:TALK37327@talks.cam.ac.uk
CONTACT:Scientific Meetings Co-ordinator
DESCRIPTION:Autoimmunity was conceptualized by Ehrlich\, who posited more 
 than 100 years ago that mechanisms for self/non-self discrimination must e
 xist in any immune system.  Today we know that recognition of non-self is 
 exercised both by the innate and by the adaptive immune systems.  Initial 
 awareness of infection is provided by the former\, and depends upon a rema
 rkably small number of molecular interactions.  In mammals\, several types
  of innate immune sensors recognize conserved molecular signatures of infe
 ction\, either on the surface of cells or within the cytosol.  These senso
 rs trigger a cytokine response that orchestrates inflammation\, including 
 the recruitment of many innate immune cells to the site of infection.  Wit
 hout this response\, a state of immune compromise exists in which the host
  is quickly overwhelmed by microbes because it lacks awareness of infectio
 n.  The Toll-like receptors (TLRs)\, an ancient family of innate immune se
 nsors\, are the most diverse in terms of ligand recognition.  Their involv
 ement in microbe sensing was discovered using a classical genetic approach
 .  It was determined that one member of the TLR family\, TLR4\, was mutate
 d in mice that could not recognize bacterial lipopolysaccharide (LPS)\, kn
 own for many years as an inducer of systemic inflammation and shock during
  Gram-negative infection.  The specificity of the other members of the TLR
  family was subsequently elucidated by reverse genetic methods.  I will re
 view these studies and consider TLR signaling pathways and the role played
  by TLRs in autoimmune and autoinflammatory diseases.
LOCATION:Max Perutz Lecture Theatre\, Medical Research Council (MRC) (MRC 
 Laboratory of Molecular Biol
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