Type 2 innate signals stimulate fibro/adipogenic progenitors to facilitate muscle regeneration

In vertebrates, activation of innate immunity is an early response to injury, implicating it in the regenerative process. However, the mechanisms by which innate signals might regulate stem cell functionality are unknown. Here, we demonstrate that type 2 innate immunity is required for regeneration...

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Vydáno v:Cell Ročník 153; číslo 2; s. 376
Hlavní autoři: Heredia, Jose E, Mukundan, Lata, Chen, Francis M, Mueller, Alisa A, Deo, Rahul C, Locksley, Richard M, Rando, Thomas A, Chawla, Ajay
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 11.04.2013
Témata:
Animals
Cobra Cardiotoxin Proteins
Eosinophils - physiology
Immunity, Innate
Interleukin-13 - genetics
Interleukin-13 - metabolism
Interleukin-4 - genetics
Interleukin-4 - metabolism
Mice
Muscle Development
Muscle, Skeletal - cytology
Muscle, Skeletal - injuries
Muscle, Skeletal - physiology
Myeloid Cells - metabolism
Receptors, Cell Surface - metabolism
Regeneration
Signal Transduction
STAT6 Transcription Factor - metabolism
ISSN:1097-4172, 1097-4172
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Popis
Shrnutí:In vertebrates, activation of innate immunity is an early response to injury, implicating it in the regenerative process. However, the mechanisms by which innate signals might regulate stem cell functionality are unknown. Here, we demonstrate that type 2 innate immunity is required for regeneration of skeletal muscle after injury. Muscle damage results in rapid recruitment of eosinophils, which secrete IL-4 to activate the regenerative actions of muscle resident fibro/adipocyte progenitors (FAPs). In FAPs, IL-4/IL-13 signaling serves as a key switch to control their fate and functions. Activation of IL-4/IL-13 signaling promotes proliferation of FAPs to support myogenesis while inhibiting their differentiation into adipocytes. Surprisingly, type 2 cytokine signaling is also required in FAPs, but not in myeloid cells, for rapid clearance of necrotic debris, a process that is necessary for timely and complete regeneration of tissues.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:1097-4172
1097-4172
DOI:10.1016/j.cell.2013.02.053