Perinatal Licensing of Thermogenesis by IL-33 and ST2

Justin I. Odegaard, Min Woo Lee, Yoshitaka Sogawa, Ambre M. Bertholet, Richard M. Locksley, David E. Weinberg, Yuriy Kirichok, Rahul C. Deo, Ajay Chawla

Research output: Contribution to journalArticlepeer-review

84 Scopus citations


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.

Original languageEnglish
Pages (from-to)841-854
Number of pages14
Issue number4
StatePublished - Aug 11 2016


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