title: Role for Toll-like receptor 3 in muscle regeneration after cardiotoxin injury.
abstract: BACKGROUND
  Sterile tissue injury induces an inflammatory response involving cytokines that have crucial roles in the tissue repair that follows.
  
  
  METHODS
  MyH3 and type 1 interferon (IFN) were assessed by qPCR after cardiotoxin (CTX)-induced muscle injury.
  
  
  RESULTS
  CTX-induced injury increased expression of IFN-regulated genes, IFIT1 and MX-2, which was blocked in type 1 IFN receptor (IFNR)-deficient mice. However, IFNR-deficient mice showed no significant differences in muscle regeneration as assessed by MyH3 expression. MyH3 was significantly reduced in TLR3-deficient but not MyD88-deficient mice. TLR3-deficient mice also showed altered expression of proinflammatory cytokines, IL-6, IL-1β, and TNF-α.
  
  
  CONCLUSIONS
  CTX-induced muscle injury increased markers of innate immune activation, but blocking type 1 IFN signaling had no effect on muscle regeneration. Taken together, these results suggest a role for TLR3, and perhaps other innate immune signals, in the inflammatory response to CTX-induced muscle injury and consequent muscle regeneration.
authors.affiliation: Rheumatology Section, Department of Medicine, Boston University School of Medicine, 72 East Concord Street, E501, Boston, Massachusetts 02118, USA.
authors.forename: Allison L
authors.initials: AL
authors.lastname: Mathes
authors.forename: Robert
authors.initials: R
authors.lastname: Lafyatis
mesh_terms: D000818:Animals; D054715:Cardiotoxins / Q000633:toxicity*; D007113:Immunity, Innate / Q000187:drug effects; D018836:Inflammation Mediators / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D018482:Muscle, Skeletal / Q000187:drug effects / Q000293:injuries* / Q000473:pathology*; D012038:Regeneration / Q000187:drug effects / Q000502:physiology*; D051196:Toll-Like Receptor 3 / Q000502:physiology*
chemical_list: D054715:Cardiotoxins; D018836:Inflammation Mediators; C519703:TLR3 protein, mouse; D051196:Toll-Like Receptor 3