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SUMMARY:Deciphering host-helminth cross talk – the battle for clearance 
 or chronicity
DTSTART:20130523T121500
DTEND:20130523T131500
DTSTAMP:20260414T132358Z
UID:d3bf2574e3c1d6e3be9ae1976a1319babb12a4bf0ad3536c634ecb83
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. Nicola Harris\nIntestinal helminth infections are the mo
 st widespread and prevalent of all parasitic diseases\, infecting one in t
 hree of the world's population. Though not usually lethal\, these parasite
 s are major causes of host morbidity particularly within children. No vacc
 ines are currently available. Our work has provided grounds for optimism i
 n the search for effective vaccines by revealing that parasite-specific an
 tibodies can control intestinal worm infection. We also showed that helmin
 ths have evolved the ability to divert the host immune response away from 
 production of ‘protective’ antibodies and towards ‘non-specific’ a
 ntibodies\, allowing parasite chronicity. These findings had clear implica
 tions for basic parasitology and for vaccine development\, yet they also h
 ighlighted how little is known about protection from these pathogens. We t
 hus undertook further work to discover the precise mechanisms through whic
 h antibodies provide anti-helminth immunity. Our first studies identified 
 a crucial role for antibodies in promoting basophil hematopoiesis within t
 he bone marrow. We additionally found that antibodies were key for macroph
 age mediated control of helminths\; specifically\, antibodies allowed macr
 ophages to adhere to tissue invasive larvae\, they modulated macrophage ge
 ne expression and reduced larval motility. Antibody-induced macrophage tra
 pping of helminth larvae functioned to prevent the parasite from completin
 g its lifecycle and acted to protect the host against extensive tissue dam
 age. Current work in our laboratory is focused on expanding these findings
  to investigate the impact of antibodies on tissue damage and repair mecha
 nisms.
LOCATION:SV 1717 A
STATUS:CONFIRMED
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