BEGIN:VCALENDAR
VERSION:2.0
PRODID:icalendar-ruby
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VTIMEZONE
TZID:Europe/Vienna
BEGIN:DAYLIGHT
DTSTART:20180325T030000
TZOFFSETFROM:+0100
TZOFFSETTO:+0200
RRULE:FREQ=YEARLY;BYDAY=-1SU;BYMONTH=3
TZNAME:CEST
END:DAYLIGHT
BEGIN:STANDARD
DTSTART:20181028T020000
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
RRULE:FREQ=YEARLY;BYDAY=-1SU;BYMONTH=10
TZNAME:CET
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTAMP:20260404T053034Z
UID:5a8ea99b44ab2375142415@ist.ac.at
DTSTART:20180406T100000
DTEND:20180406T110000
DESCRIPTION:Speaker: Federica Benvenuti\nhosted by Michael Sixt\nAbstract: 
 Dendritic cells are central to initiate responses to viruses and transform
 ed cells. In the lab we focus on pathological contexts where DCs functions
  are deviated from normal\, trying to understand the underlying cell biolo
 gical mechanism.In DCs derived from a mouse model of Wiskott-Aldrich syndr
 ome\, a rare primary immune deficiency\, lack of the actin nucleation-prom
 oting factor WASp causes defects in cell migration and interaction with T 
 cells. In addition to this established cellular defects\, we discovered th
 at signalling from endosomal Toll-like receptor 9 is enhanced in WASp null
  cells\, leading to excessive production of type-I interferon and chronic 
 inflammation. We investigated the basis of excessive signalling by trackin
 g the intracellular journey of TLR9 ligands and the overall morphology and
  function of the endocytic system. We found that WASp controls endo-lysoso
 mal fusion and delivery of endocytic cargo to lysosomes for degradation. L
 ack of WASp\, or chemical inhibition of Arp2/3\, causes accumulation of ca
 rgo and receptor and lowers the threshold for receptor activation. These f
 indings help to explain the enhanced sensitivity to low amount of innate t
 riggers and the susceptibility to develop autoimmune phenomena in Wiskott-
 Aldrich syndrome. A second interest of the lab is to understand the mechan
 isms of DC suppression in lung tumors. We have found that lung tissue resi
 dent type-1 DCs\, specialized in cross-presentation of antigens\, loose th
 e capacity to activate CD8+ T cells in tumors. Transcriptomic analysis of 
 lung tumor-associated DC1 showed changes in pathways of antigen uptake and
  intracellular trafficking. Loss of a specific phosphatydilserine receptor
  suggests that cancer cell may escape immune recognition by targeting upta
 ke and acquisition of tumor antigens by DC1\, an essential step in priming
  of anti-tumor T cell responses.
LOCATION:Mondi Seminar Room 2\, Central Building\, ISTA
ORGANIZER:astawick@ist.ac.at
SUMMARY:Federica Benvenuti: WASp mediated Arp2/3 activation controls endo-l
 ysosomal fusion and cargo degradation determining the threshold for Toll-l
 ike receptor 9 activation
URL:https://talks-calendar.ista.ac.at/events/1176
END:VEVENT
END:VCALENDAR