IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2

Emily L. Goldberg, Irina Shchukina, Yun Hee Youm, Seungjin Ryu, Takeshi Tsusaka, Kyrlia C. Young, Christina D. Camell, Tamara Dlugos, Maxim N. Artyomov, Vishwa Deep Dixit

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Aging impairs the integrated immunometabolic responses, which have evolved to maintain core body temperature in homeotherms to survive cold stress, infections, and dietary restriction. Adipose tissue inflammation regulates the thermogenic stress response, but how adipose tissue-resident cells instigate thermogenic failure in the aged are unknown. Here, we define alterations in the adipose-resident immune system and identify that type 2 innate lymphoid cells (ILC2s) are lost in aging. Restoration of ILC2 numbers in aged mice to levels seen in adults through IL-33 supplementation failed to rescue old mice from metabolic impairment and increased cold-induced lethality. Transcriptomic analyses revealed intrinsic defects in aged ILC2, and adoptive transfer of adult ILC2s are sufficient to protect old mice against cold. Thus, the functional defects in adipose ILC2s during aging drive thermogenic failure.

Original languageEnglish
Pages (from-to)2277-2287.e5
JournalCell metabolism
Issue number11
StatePublished - Nov 2 2021


  • IL-33
  • ILC2
  • adipose
  • aging
  • inflammation
  • metabolism
  • thermogenesis


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