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SUMMARY:Tolerogenic dendritic cells in chronic helminth infection - Dr Kat
 ie Smith\, Institute of Infection and Immunology Research\, University of 
 Edinburgh
DTSTART:20090506T113000Z
DTEND:20090506T123000Z
UID:TALK17895@talks.cam.ac.uk
CONTACT:Prof. Jim Kaufman
DESCRIPTION:Parasites have evolved effective mechanisms to manipulate an i
 mmune response and prevent expulsion from the host. Most notably\, some gu
 t helminths can also downregulate T cell responses to inflammatory stimuli
  including asthmatic and allergic reactions through stimulation and expans
 ion of Foxp3+ regulatory T cells. Experiments in our lab have shown that F
 oxp3+ regulatory T cell expansion in vitro can be linked to a TGF-beta-lik
 e activity present in the excretory/secretory products of the rodent gut h
 elminth Heligmosomoides Polygyrus. Chronic persistence of the adult worm i
 nfection can be modified by use of a synthetic TGF-beta type 1 receptor in
 hibitor in vivo. \n\nI am interested in the mechanisms underlying this Fox
 p3+ regulatory T cell expansion in vivo and have focused on whether antige
 n presenting cells such as dendritic cells are re-programmed to a toleroge
 nic\, regulatory T cell inducing\, phenotype following infection. I have f
 ound that chronic helminth infection is associated with the expansion of C
 D11c(lo) dendritic cells in the draining lymph nodes of the gut. These cel
 ls have a plasmacytoid dendritic cell phenotype\, a distinct response to T
 LR ligation and present antigen to T cells far less efficiently on compari
 son to conventional CD11c(hi) dendritic cells. CD11c(lo) cells polarise na
 ive T cells to distinct T cells lineages\, encouraging the expansion of an
 tigen-specific Foxp3 T cells and polarisation away from Th17 cells. These 
 regulatory T cell changes could be inhibited with excess antigen or the re
 tinoic acid receptor antagonist LE540 and are enhanced with recombinant TG
 F-beta. My research is now focusing on manipulating plasmacytoid dendritic
  cell populations in vivo and determining the cause for the changes in the
  CDllc(lo) and Foxp3+ T cell populations following infection. Ultimately\,
  my interest is in understanding the immunological mechanisms underlying h
 elminth persistence\, to determine whether these conditions can be replica
 ted to drive tolerance in vivo.\n
LOCATION:Lecture Theater\, Department of Pathology\, Tennis Court Road
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