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

Cervera Álvarez, ÁlvaroPlanas Obradors, Anna MariaJusticia Mercader, CarlesUrra, XabierJensenius, Jens C.Torres Peraza, Jesús FernandoLozano Soto, FranciscoChamorro Sánchez, Ángel2013-06-032013-06-032010-021932-6203https://hdl.handle.net/2445/44003The 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.10 p.application/pdfengcc-by (c) Cervera Álvarez, Álvaro et al., 2010http://creativecommons.org/licenses/by/3.0/esEnzims proteolíticsInfart cerebralImmunitatModels animals en la investigacióProteolytic enzymesCerebral infarctioImmunityAnimal models in researchGenetically-defined deficiency of mannose-binding lectin is associated with protection after experimental stroke in mice and outcome in human strokeinfo:eu-repo/semantics/article5985532013-06-03info:eu-repo/semantics/openAccess20140243