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Cell. 2016 Aug 11;166(4):841-854. doi: 10.1016/j.cell.2016.06.040. Epub 2016 Jul 21.

Perinatal Licensing of Thermogenesis by IL-33 and ST2.

Author information

1
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA.
2
Department of Physiology, University of California, San Francisco, San Francisco, CA 94143-0795, USA.
3
Department of Medicine, University of California, San Francisco, San Francisco, CA 94143-0795, USA; Department Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143-0795, USA; Howard Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA.
4
Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94143-0795, USA.
5
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA; Department of Medicine, University of California, San Francisco, San Francisco, CA 94143-0795, USA.
6
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143-0795, USA; Department of Physiology, University of California, San Francisco, San Francisco, CA 94143-0795, USA; Department of Medicine, University of California, San Francisco, San Francisco, CA 94143-0795, USA. Electronic address: ajay.chawla@ucsf.edu.

Abstract

For placental mammals, the transition from the in utero maternal environment to postnatal life requires the activation of thermogenesis to maintain their core temperature. This is primarily accomplished by induction of uncoupling protein 1 (UCP1) in brown and beige adipocytes, the principal sites for uncoupled respiration. Despite its importance, how placental mammals license their thermogenic adipocytes to participate in postnatal uncoupled respiration is not known. Here, we provide evidence that the "alarmin" IL-33, a nuclear cytokine that activates type 2 immune responses, licenses brown and beige adipocytes for uncoupled respiration. We find that, in absence of IL-33 or ST2, beige and brown adipocytes develop normally but fail to express an appropriately spliced form of Ucp1 mRNA, resulting in absence of UCP1 protein and impairment in uncoupled respiration and thermoregulation. Together, these data suggest that IL-33 and ST2 function as a developmental switch to license thermogenesis during the perinatal period. PAPERCLIP.

PMID:
27453471
PMCID:
PMC4985267
DOI:
10.1016/j.cell.2016.06.040
[Indexed for MEDLINE]
Free PMC Article

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