Jens Christian Jensenius

Genetically-defined deficiency of mannose-binding lectin is associated with protection after experimental stroke in mice and outcome in human stroke

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

  • Alvaro Cervera
  • ,
  • Anna M Planas
  • ,
  • Carles Justicia
  • ,
  • Xabier Urra
  • ,
  • Jens Christian Jensenius
  • Ferran Torres
  • ,
  • Francisco Lozano
  • ,
  • Angel Chamorro
The complement system is a major effector of innate immunity that has been involved in stroke brain damage. Complement activation occurs through the classical, alternative and lectin pathways. The latter is initiated by mannose-binding lectin (MBL) and MBL-associated serine proteases (MASPs). Here we investigated whether the lectin pathway contributes to stroke outcome in mice and humans.
Original languageEnglish
JournalP L o S One
Pages (from-to)e8433
Publication statusPublished - 2010

    Research areas

  • Aged, Aged, 80 and over, Animals, Blotting, Western, Brain Ischemia, Cell Line, Complement C3, Female, Genotype, Humans, Immunohistochemistry, Logistic Models, Male, Mannose-Binding Lectin, Mannose-Binding Protein-Associated Serine Proteases, Mice, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, Recombinant Proteins, Signal Transduction, Stroke

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