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SUMMARY:The lectin pathway of complement: The Swiss army knife of innate i
 mmunity - Professor Peter Garred\, Faculty of Health and Medical Sciences\
 , University of Copenhagen
DTSTART:20191127T160000Z
DTEND:20191127T170000Z
UID:TALK126232@talks.cam.ac.uk
CONTACT:Fiona Roby
DESCRIPTION:Mannose-binding lectin (MBL)\, collectin-10\, collectin-11 and
  the ficolins (ficolin-1\, ficolin-2 and ficolin-3) are soluble pattern re
 cognition molecules in the lectin complement pathway. These proteins act a
 s mediators of host defense and participate in maintenance of tissue homeo
 stasis. They bind to conserved pathogen-specific structures and altered-se
 lf antigens and form complexes with the pentraxins to modulate innate immu
 ne functions. All molecules exhibit distinct expression in different tissu
 e compartments\, but all are found to a varying degree in the circulation.
  A common feature of these molecules is their ability to interact with a s
 et of serine proteases named MASPs (MASP-1\, MASP-2 and MASP-3). MASP-1 an
 d -2 trigger the activation of the lectin pathway and MASP-3 is involved i
 n the activation of the alternative pathway of complement. Furthermore\, M
 ASPs mediate processes related to coagulation\, bradykinin release\, endot
 helial and platelet activation. Variant alleles affecting expression and s
 tructure of the proteins have been associated with a variety of infectious
  and non-infectious diseases\, most commonly as disease modifiers. Notably
 \, the severe 3MC (Malpuech\, Michels\, Mingarelli and Carnevale) embryoni
 c development syndrome originates from rare mutations affecting either col
 lectin-10\, collectin-11 or MASP-3\, indicating a broader functionality of
  the complement system than previously anticipated. The lectin pathway has
  been shown to be driver in many inflammatory diseases\, which makes thera
 peutic intervention a feasible option.
LOCATION:Lecture Theatre 2\, Department of Veterinary Medicine
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