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DTSTAMP:20120406T174847Z
DTSTART;TZID=America/Los_Angeles:20120413T160000
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TRANSP:OPAQUE
SUMMARY:Direct benefit of acute inflammation in corneal wound healing *Note: actual end time may vary.* 
UID:54624-ucb-events-calendar@berkeley.edu
ORGANIZER;CN="UC Berkeley Calendar Network":
LOCATION:489 Minor Hall
DESCRIPTION:C. Wayne Smith\, MD\, Baylor College of Medicine\n\nEfficient wound healing of the cornea involves restoration of surface epithelium and regeneration of the subepithelial sensory nerve plexus. A mouse model of corneal epithelial abrasion reveals an acute inflammatory response in the limbal vessels involving immigration of lymphocytes\, neutrophils\, monocytes and platelets. The most abundant lymphocytes accumulating in the corneal epithelium after injury are T cells dependent on epithelial production of CCL20\, and NK cells dependent on CXCL10. The γδ T cells are a IL-17A+ IL-22+ CCR6+ subset important for the inflammatory response to injury\, and the NK cells are a CD3— IL-22— CD94— NKG2D+ subset involved in limiting the acute inflammatory response to injury. IL-17A and IL-22 stimulate corneal epithelial proliferation and migration\, and they promote corneal accumulation of neutrophils and platelets\, cells containing for example VEGF-A\, a trophic factor for early neurite regeneration. Thus\, γδ T cells\, neutrophils and platelets are all necessary for efficient epithelial closure and nerve regeneration. However\, excessive inflammation interferes with healing. NK cells appear to limit the innate acute inflammatory cascade since NK cell depletion results in prolonged accumulation of neutrophils\, delayed wound closure and delayed nerve regeneration. These studies indicate two dominant subsets of lymphocytes that allow a balanced\, pro-healing innate acute inflammatory response.
URL:http://events.berkeley.edu/index.php/calendar/sn/pubaff.html?event_ID=54624&view=preview
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