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SUMMARY:Microglia as modulators of CNS inflammation - Trevor Owens\, Unive
 rsity of Southern Denmark
DTSTART:20210510T150000Z
DTEND:20210510T160000Z
UID:TALK160198@talks.cam.ac.uk
CONTACT:47293
DESCRIPTION:Microglia\, as tissue resident macrophages of the CNS\, play i
 mportant roles in development and maintaining homeostasis. Heterogeneity o
 f these autonomously self-renewing myeloid cells reflects plasticity in re
 sponse to microenvironmental changes which include aging\, inflammation\, 
 degeneration and injury. Nevertheless transcriptomic signatures from a num
 ber of studies show similar overlapping microglial gene expression pattern
 s in homeostasis as well as in disease or injury\, and a core signature fo
 r a unique subset can be identified. Tracking this subset based on CD11c e
 xpression revealed homeostatic and anti-inflammatory characteristics which
  could be exploited for amelioration of EAE in adult mice by expansion of 
 this subset by CSF1R ligands. Myelination in early postnatal CNS is promot
 ed by IGF1 deriving from CD11c+ microglia and data will be presented showi
 ng that transfer of neonatal microglia to adult mice suppressed EAE. In a 
 mouse model for NMOSD induced by transfer of patient-derived IgG\, microgl
 ia (including the CD11c+ subset) showed a strong type I IFN transcriptomic
  footprint\, and consistent with NMOSD being IFN I-dependent\, microglial 
 depletion abrogated both IFN I-induced gene expression as well as prevente
 d induction of NMOSD pathology. Taken together\, these findings provide a 
 glimpse into the context-dependent complexity of microglial modulation of 
 CNS homeostasis.
LOCATION:https://zoom.us/j/96376288428?pwd=bUE2SU90eXAyQnVqV3BkVG14TUZEdz0
 9
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