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Research output: Contribution to Journal/Magazine › Journal article › peer-review
Local amplifiers of IL-4Rα-mediated macrophage activation promote repair in lung and liver. / Minutti, Carlos M; Jackson-Jones, Lucy H; García-Fojeda, Belén et al.
In: Science, Vol. 356, No. 6342, 09.06.2017, p. 1076-1080.Research output: Contribution to Journal/Magazine › Journal article › peer-review
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TY - JOUR
T1 - Local amplifiers of IL-4Rα-mediated macrophage activation promote repair in lung and liver
AU - Minutti, Carlos M
AU - Jackson-Jones, Lucy H
AU - García-Fojeda, Belén
AU - Knipper, Johanna A
AU - Sutherland, Tara E
AU - Logan, Nicola
AU - Ringqvist, Emma
AU - Guillamat-Prats, Raquel
AU - Ferenbach, David A
AU - Artigas, Antonio
AU - Stamme, Cordula
AU - Chroneos, Zissis C
AU - Zaiss, Dietmar M
AU - Casals, Cristina
AU - Allen, Judith E
N1 - Copyright © 2017, American Association for the Advancement of Science.
PY - 2017/6/9
Y1 - 2017/6/9
N2 - 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 interleukin-4 (IL-4)-dependent macrophage proliferation and activation, accelerating parasite clearance and reducing pulmonary injury after infection with a lung-migrating helminth. In the peritoneal cavity and liver, C1q enhancement of type 2 macrophage activation was required for liver repair after bacterial infection, but resulted in fibrosis after 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.
AB - 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 interleukin-4 (IL-4)-dependent macrophage proliferation and activation, accelerating parasite clearance and reducing pulmonary injury after infection with a lung-migrating helminth. In the peritoneal cavity and liver, C1q enhancement of type 2 macrophage activation was required for liver repair after bacterial infection, but resulted in fibrosis after 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.
KW - Animals
KW - Complement C1q
KW - Humans
KW - Interleukin-4
KW - Listeria monocytogenes
KW - Listeriosis
KW - Liver
KW - Lung
KW - Macrophage Activation
KW - Mice
KW - Mice, Inbred C57BL
KW - Nippostrongylus
KW - Pulmonary Surfactant-Associated Protein A
KW - Receptors, Interleukin-4
KW - Regeneration
KW - Strongylida Infections
KW - Journal Article
KW - Research Support, N.I.H., Extramural
KW - Research Support, Non-U.S. Gov't
U2 - 10.1126/science.aaj2067
DO - 10.1126/science.aaj2067
M3 - Journal article
C2 - 28495878
VL - 356
SP - 1076
EP - 1080
JO - Science
JF - Science
SN - 0036-8075
IS - 6342
ER -