Reference

DOI: 10.1126/science.aaj2067 science

Authors

Carlos M. Minutti, Lucy Jackson-Jones, Belén García-Fojeda, Johanna Knipper, Tara Sutherland, Nicola Logan, Emma Rinqvist, Raquel Guillamat-Prats, David Ferenbach, Antonio Artigas, Cordula Stamme, Zissis C. Chroneos, Dietmar M. Zaiss, Cristina Casals y Judith E. Allen.

Abstract

The type 2 immune response controls helminth infection and maintains tissue homeostasis but can lead to allergy and fibrosis if not adequately regulated. We have discovered local tissue-specific amplifiers of type-2 mediated-macrophage activation. In the lung, surfactant protein A (SP-A) enhanced IL-4-dependent macrophage proliferation and activation, accelerating parasite clearance and reducing pulmonary injury following infection with a lung-migrating helminth. In the peritoneal cavity and liver, C1q enhancement of type 2 macrophage activation was required for liver repair following bacterial infection, but resulted in fibrosis following peritoneal dialysis. IL-4 drives production of these structurally related defense collagens, SP-A and C1q, and the expression of their receptor, myosin 18A. These findings reveal the existence within different tissues of an amplification system needed for local type 2 responses.

Description

Nuestro estudio demuestra la existencia de amplificadores específicos de tejido necesarios para promover la activación y proliferación de macrófagos mediada por IL-4Ra. IL-4 da lugar a la producción de proteínas estructuralmente similares, SP-A en pulmón y C1q en hígado, y a la expresión de su receptor (myosin 18A), impulsando la activación efectiva de macrófagos para frenar la lesión y favorecer la reparación del tejido después de la infección con parásitos o bacterias patógenas.

 

 

Carlos Minutti C Casals B Garcia Fojeda 4

 

REFERENCIA DEL GRUPO INVESTIGADOR

Uno de los objetivos del grupo de la Profesora Cristina Casals (Dept. de Bioquímica y Biología Molecular de la Universidad Complutense de Madrid y del CIBER de Enfermedades Respiratorias) es estudiar los mecanismos moleculares por los que lípidos y proteínas presentes en el fluido alveolar controlan la infección e inflamación y promueven la reparación del tejido después del daño.

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