La hipoxia induce la activación de los macrófagos potenciando la fagocitosis y la presentación antigénica, a través de la producción de IFN- gamma, mediada por el factor de transcripción HIF-1 alfa

• Autores: Bárbara Acosta Iborra
• Directores de la Tesis: Isabel María Olazábal Olarreaga (dir. tes.), Manuel Ortiz (dir. tes.)
• Lectura: En la Universidad Autónoma de Madrid ( España ) en 2009
• Idioma: español
• Tribunal Calificador de la Tesis: Manuel Fresno Escudero (presid.), Miguel Ángel Íñiguez Peña (secret.), Laura García Bermejo (voc.), Ángel L. Corbí López (voc.), Gemma Olmos Centenera (voc.)
• Materias:
  • Ciencias de la vida
    • Biología molecular
• Enlaces
  • Tesis en acceso abierto en: Biblos-e Archivo
• Resumen

  • Low oxygen tension areas are found in inflamed or diseased tissues where hypoxic cells induce survival pathways by regulating the hypoxia-inducible transcription factor (HIF). Macrophages are essential regulators of inflammation and, therefore, we have analyzed their response to hypoxia. Murine peritoneal elicited macrophages cultured under hypoxia produced higher levels of IFN-g and IL-12 mRNA and protein than those cultured under normoxia. A similar IFN- g increment was obtained with in vivo models using macrophages from mice exposed to atmospheric hypoxia. Our studies showed that IFN-g induction was mediated through HIF-1a binding to its promoter on a new functional hypoxia response element. The requirement of HIF-1a in the IFN-g induction was confirmed in RAW264.7 cells, where HIF-1a was knocked down, as well as in resident HIF-1a null macrophages.