Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Review Article
  • Published:

Metabolic control of innate lymphoid cells in health and disease

Nature Metabolism volume 4, pages 1650–1659 (2022)Cite this article

Subjects

Abstract

Innate lymphoid cells (ILCs) are a family of predominantly tissue-resident lymphocytes that critically orchestrate immunity, inflammation, tolerance and repair at barrier surfaces of the mammalian body. Heterogeneity among ILC subsets is comparable to that of adaptive CD4+ T helper cell counterparts, and emerging studies demonstrate that ILC biology is also dictated by cellular metabolism that adapts bioenergetic requirements during activation, proliferation or cytokine production. Accumulating evidence in mouse models and human samples indicates that ILCs exhibit profound roles in shaping states of metabolic health and disease. Here we summarize and discuss our current knowledge of the cell-intrinsic and cell-extrinsic metabolic factors controlling ILC responses, as well as highlight contributions of ILCs to organismal metabolism. It is expected that continued research in this area will advance our understanding of how to manipulate ILCs or their metabolism for therapeutic strategies that benefit human health.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Fig. 1: Cell-intrinsic metabolic pathways employed by the ILC family.
Fig. 2: Metabolic regulation of ILC responses by external environmental cues.
Fig. 3: Regulation of host metabolic physiology by ILCs.

Similar content being viewed by others

References

  1. Vivier, E. et al. Innate lymphoid cells: 10 years on. Cell 174, 1054–1066 (2018).

    Article  CAS  Google Scholar 

  2. Spits, H. et al. Innate lymphoid cells—a proposal for uniform nomenclature. Nat. Rev. Immunol. 13, 145–149 (2013).

    Article  CAS  Google Scholar 

  3. Artis, D. & Spits, H. The biology of innate lymphoid cells. Nature 517, 293–301 (2015).

    Article  CAS  Google Scholar 

  4. Klose, C. S. & Artis, D. Innate lymphoid cells as regulators of immunity, inflammation and tissue homeostasis. Nat. Immunol. 17, 765–774 (2016).

    Article  CAS  Google Scholar 

  5. Zhou, L. & Sonnenberg, G. F. Essential immunologic orchestrators of intestinal homeostasis. Sci. Immunol. https://doi.org/10.1126/sciimmunol.aao1605 (2018).

  6. Zhou, L. et al. Innate lymphoid cells support regulatory T cells in the intestine through interleukin-2. Nature 568, 405–409 (2019).

    Article  CAS  Google Scholar 

  7. Zhou, L. et al. Group 3 innate lymphoid cells produce the growth factor HB-EGF to protect the intestine from TNF-mediated inflammation. Nat. Immunol. 23, 251–261 (2022).

    Article  CAS  Google Scholar 

  8. Lyu, M. et al. ILC3s select microbiota-specific regulatory T cells to establish tolerance in the gut. Nature https://doi.org/10.1038/s41586-022-05141-x (2022).

    Article  Google Scholar 

  9. Zhou, W. et al. ZBTB46 defines and regulates ILC3s that protect the intestine. Nature 609, 159–165 (2022).

    Article  CAS  Google Scholar 

  10. Ouyang, W. & O’Garra, A. IL-10 family cytokines IL-10 and IL-22: from basic science to clinical translation. Immunity 50, 871–891 (2019).

    Article  CAS  Google Scholar 

  11. Dudakov, J. A., Hanash, A. M. & van den Brink, M. R. Interleukin-22: immunobiology and pathology. Annu. Rev. Immunol. 33, 747–785 (2015).

    Article  CAS  Google Scholar 

  12. Huang, Y. et al. IL-25-responsive, lineage-negative KLRG1hi cells are multipotential ‘inflammatory’ type 2 innate lymphoid cells. Nat. Immunol. 16, 161–169 (2015).

    Article  CAS  Google Scholar 

  13. Grigg, J. B. et al. Antigen-presenting innate lymphoid cells orchestrate neuroinflammation. Nature 600, 707–712 (2021).

    Article  CAS  Google Scholar 

  14. Buck, M. D., O’Sullivan, D. & Pearce, E. L. T cell metabolism drives immunity. J. Exp. Med. 212, 1345–1360 (2015).

    Article  CAS  Google Scholar 

  15. Geltink, R. I. K., Kyle, R. L. & Pearce, E. L. Unraveling the complex interplay between T cell metabolism and function. Annu. Rev. Immunol. 36, 461–488 (2018).

    Article  CAS  Google Scholar 

  16. Chapman, N. M., Boothby, M. R. & Chi, H. Metabolic coordination of T cell quiescence and activation. Nat. Rev. Immunol. 20, 55–70 (2020).

    Article  CAS  Google Scholar 

  17. O’Brien, K. L. & Finlay, D. K. Immunometabolism and natural killer cell responses. Nat. Rev. Immunol. 19, 282–290 (2019).

    Article  Google Scholar 

  18. Terren, I. et al. Modulating NK cell metabolism for cancer immunotherapy. Semin. Hematol. 57, 213–224 (2020).

    Article  Google Scholar 

  19. Gury-BenAri, M. et al. The spectrum and regulatory landscape of intestinal innate lymphoid cells are shaped by the microbiome. Cell 166, 1231–1246 (2016).

    Article  CAS  Google Scholar 

  20. Monticelli, L. A. et al. Arginase 1 is an innate lymphoid-cell-intrinsic metabolic checkpoint controlling type 2 inflammation. Nat. Immunol. 17, 656–665 (2016). This paper details arginase 1 as a key metabolic checkpoint that is required to meet the bioenergetic needs of ILC2s during type 2 inflammation.

    Article  CAS  Google Scholar 

  21. Bando, J. K., Nussbaum, J. C., Liang, H. E. & Locksley, R. M. Type 2 innate lymphoid cells constitutively express arginase 1 in the naive and inflamed lung. J. Leukoc. Biol. 94, 877–884 (2013).

    Article  CAS  Google Scholar 

  22. Wilhelm, C. et al. Critical role of fatty acid metabolism in ILC2-mediated barrier protection during malnutrition and helminth infection. J. Exp. Med. 213, 1409–1418 (2016). This paper determined that ILC2s robustly utilize fatty acid metabolism for IL-13 production during helminth infection.

    Article  CAS  Google Scholar 

  23. Karagiannis, F. et al. Lipid-droplet formation drives pathogenic group 2 innate lymphoid cells in airway inflammation. Immunity 52, 620–634 (2020). This paper identifies that pro-inflammatory ILC2 responses in the airway are regulated by IL-33-induced Pparg and Dgat that subsequently support lipid droplet storage and fatty acid metabolism.

    Article  CAS  Google Scholar 

  24. Surace, L. et al. Dichotomous metabolic networks govern human ILC2 proliferation and function. Nat. Immunol. 22, 1367–1374 (2021). This paper details how human ILC2s exhibit differential dependence of OXPHOS and mTOR signaling for proliferation and cytokine production, respectively.

    Article  CAS  Google Scholar 

  25. Galle-Treger, L. et al. Autophagy is critical for group 2 innate lymphoid cell metabolic homeostasis and effector function. J. Allergy Clin. Immunol. 145, 502–517 (2020).

    Article  CAS  Google Scholar 

  26. Helou, D. G. et al. PD-1 pathway regulates ILC2 metabolism and PD-1 agonist treatment ameliorates airway hyperreactivity. Nat. Commun. 11, 3998 (2020).

    Article  CAS  Google Scholar 

  27. Fu, L. et al. A mitochondrial STAT3–methionine metabolism axis promotes ILC2-driven allergic lung inflammation. J. Allergy Clin. Immunol. https://doi.org/10.1016/j.jaci.2021.12.783 (2021).

    Article  Google Scholar 

  28. Hodge, S. H. et al. Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses. Preprint at BioRxiv https://doi.org/10.1101/2022.06.22.497162 (2022).

  29. Flamar, A. L. et al. Interleukin-33 induces the enzyme tryptophan hydroxylase 1 to promote inflammatory group 2 innate lymphoid cell-mediated immunity. Immunity 52, 606–619 (2020).

    Article  CAS  Google Scholar 

  30. Ricardo-Gonzalez, R. R. et al. Tissue signals imprint ILC2 identity with anticipatory function. Nat. Immunol. 19, 1093–1099 (2018).

    Article  CAS  Google Scholar 

  31. Di Luccia, B., Gilfillan, S., Cella, M., Colonna, M. & Huang, S. C. ILC3s integrate glycolysis and mitochondrial production of reactive oxygen species to fulfill activation demands. J. Exp. Med. 216, 2231–2241 (2019). This paper determined that ILC3s rely on mTORC1 signaling, activation of HIF1α, and mROS production to support optimal responses during an enteric infection.

    Article  Google Scholar 

  32. Budda, S. A., Girton, A., Henderson, J. G. & Zenewicz, L. A. Transcription factor HIF1α controls expression of the cytokine IL-22 in CD4+ T cells. J. Immunol. 197, 2646–2652 (2016).

  33. Dang, E. V. et al. Control of TH17/Treg balance by hypoxia-inducible factor 1. Cell 146, 772–784 (2011).

    Article  CAS  Google Scholar 

  34. Teufel, C. et al. mTOR signaling mediates ILC3-driven immunopathology. Mucosal Immunol. 14, 1323–1334 (2021).

    Article  CAS  Google Scholar 

  35. Fachi, J. L. et al. Hypoxia enhances ILC3 responses through HIF1α-dependent mechanism. Mucosal Immunol. 14, 828–841 (2021).

    Article  CAS  Google Scholar 

  36. Krzywinska, E. et al. The transcription factor HIF1α mediates plasticity of NKp46+ innate lymphoid cells in the gut. J. Exp. Med. https://doi.org/10.1084/jem.20210909 (2022). This paper identifies that intracellular metabolic networks, such as those driven by HIF1α and glycolysis, shape the plasticity ILC3 subsets.

  37. Parker, M. E. et al. c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program. J. Exp. Med. https://doi.org/10.1084/jem.20191030 (2020).

  38. Wu, D. et al. PD-1 signaling facilitates activation of lymphoid tissue inducer cells by restraining fatty acid oxidation. Nat. Metab. 4, 867–882 (2022). This paper details how PD-1 signaling impacts the cellular metabolism of an ILC3 subset and shapes effector IL-22 production during intestinal inflammation.

    Article  CAS  Google Scholar 

  39. Serafini, N. et al. Trained ILC3 responses promote intestinal defense. Science 375, 859–863 (2022).

    Article  CAS  Google Scholar 

  40. Godinho-Silva, C. et al. Light-entrained and brain-tuned circadian circuits regulate ILC3s and gut homeostasis. Nature 574, 254–258 (2019).

    Article  CAS  Google Scholar 

  41. Teng, F. et al. A circadian clock is essential for homeostasis of group 3 innate lymphoid cells in the gut. Sci. Immunol. https://doi.org/10.1126/sciimmunol.aax1215 (2019).

  42. Wang, Q. et al. Circadian rhythm-dependent and circadian rhythm-independent impacts of the molecular clock on type 3 innate lymphoid cells. Sci. Immunol. https://doi.org/10.1126/sciimmunol.aay7501 (2019).

  43. Spencer, S. P. et al. Adaptation of innate lymphoid cells to a micronutrient deficiency promotes type 2 barrier immunity. Science 343, 432–437 (2014).

    Article  CAS  Google Scholar 

  44. Mielke, L. A. et al. Retinoic acid expression associates with enhanced IL-22 production by γδ T cells and innate lymphoid cells and attenuation of intestinal inflammation. J. Exp. Med. 210, 1117–1124 (2013).

    Article  CAS  Google Scholar 

  45. van de Pavert, S. A. et al. Maternal retinoids control type 3 innate lymphoid cells and set the offspring immunity. Nature 508, 123–127 (2014).

    Article  Google Scholar 

  46. Kim, M. H., Taparowsky, E. J. & Kim, C. H. Retinoic acid differentially regulates the migration of innate lymphoid cell subsets to the gut. Immunity 43, 107–119 (2015).

    Article  CAS  Google Scholar 

  47. Konya, V. et al. Vitamin D downregulates the IL-23 receptor pathway in human mucosal group 3 innate lymphoid cells. J. Allergy Clin. Immunol. 141, 279–292 (2018).

    Article  CAS  Google Scholar 

  48. Lin, Y. D., Arora, J., Diehl, K., Bora, S. A. & Cantorna, M. T. Vitamin D is required for ILC3-derived IL-22 and protection from Citrobacter rodentium infection. Front. Immunol. 10, 1 (2019).

    Article  Google Scholar 

  49. Kiss, E. A. et al. Natural aryl hydrocarbon receptor ligands control organogenesis of intestinal lymphoid follicles. Science 334, 1561–1565 (2011).

    Article  CAS  Google Scholar 

  50. Lee, J. S. et al. AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch. Nat. Immunol. 13, 144–151 (2011).

    Article  Google Scholar 

  51. Qiu, J. et al. The aryl hydrocarbon receptor regulates gut immunity through modulation of innate lymphoid cells. Immunity 36, 92–104 (2012).

    Article  CAS  Google Scholar 

  52. Zelante, T. et al. Tryptophan catabolites from microbiota engage aryl hydrocarbon receptor and balance mucosal reactivity via interleukin-22. Immunity 39, 372–385 (2013).

    Article  CAS  Google Scholar 

  53. Li, S. et al. Aryl hydrocarbon receptor signaling cell intrinsically inhibits intestinal group 2 innate lymphoid cell function. Immunity 49, 915–928 (2018).

    Article  CAS  Google Scholar 

  54. Zhang, L. H., Shin, J. H., Haggadone, M. D. & Sunwoo, J. B. The aryl hydrocarbon receptor is required for the maintenance of liver-resident natural killer cells. J. Exp. Med. 213, 2249–2257 (2016).

    Article  CAS  Google Scholar 

  55. Chun, E. et al. Metabolite-sensing receptor Ffar2 regulates colonic group 3 innate lymphoid cells and gut immunity. Immunity 51, 871–884 (2019).

    Article  CAS  Google Scholar 

  56. Fachi, J. L. et al. Acetate coordinates neutrophil and ILC3 responses against C. difficile through FFAR2. J. Exp. Med. https://doi.org/10.1084/jem.20190489 (2020).

  57. Yang, W. et al. Intestinal microbiota-derived short-chain fatty acids regulation of immune cell IL-22 production and gut immunity. Nat. Commun. 11, 4457 (2020).

    Article  CAS  Google Scholar 

  58. Thio, C. L., Chi, P. Y., Lai, A. C. & Chang, Y. J. Regulation of type 2 innate lymphoid cell-dependent airway hyperreactivity by butyrate. J. Allergy Clin. Immunol. 142, 1867–1883 (2018).

    Article  CAS  Google Scholar 

  59. Lewis, G. et al. Dietary fiber-induced microbial short-chain fatty acids suppress ILC2-dependent airway inflammation. Front. Immunol. 10, 2051 (2019).

    Article  CAS  Google Scholar 

  60. Li, Y. et al. Natural killer cells: friend or foe in metabolic diseases. Front. Immunol. 12, 614429 (2021).

    Article  CAS  Google Scholar 

  61. O’Sullivan, T. E. et al. Adipose-resident group 1 innate lymphoid cells promote obesity-associated insulin resistance. Immunity 45, 428–441 (2016).

    Article  Google Scholar 

  62. Molofsky, A. B. et al. Interleukin-33 and interferon-γ counter-regulate group 2 innate lymphoid cell activation during immune perturbation. Immunity 43, 161–174 (2015).

    Article  CAS  Google Scholar 

  63. Boulenouar, S. et al. Adipose type one innate lymphoid cells regulate macrophage homeostasis through targeted cytotoxicity. Immunity 46, 273–286 (2017).

    Article  CAS  Google Scholar 

  64. Wang, H. et al. Adipose group 1 innate lymphoid cells promote adipose tissue fibrosis and diabetes in obesity. Nat. Commun. 10, 3254 (2019).

    Article  Google Scholar 

  65. Cuff, A. O. et al. The obese liver environment mediates conversion of NK cells to a less cytotoxic ILC1-like phenotype. Front. Immunol. 10, 2180 (2019).

    Article  CAS  Google Scholar 

  66. Hildreth, A. D. et al. Single-cell sequencing of human white adipose tissue identifies new cell states in health and obesity. Nat. Immunol. 22, 639–653 (2021).

    Article  CAS  Google Scholar 

  67. Moro, K. et al. Innate production of TH2 cytokines by adipose tissue-associated c-Kit+Sca-1+ lymphoid cells. Nature 463, 540–544 (2010). This is one of the seminal reports defining ILC2s and reveals their intimate association with adipose tissues.

    Article  CAS  Google Scholar 

  68. Hams, E., Locksley, R. M., McKenzie, A. N. & Fallon, P. G. Cutting edge: IL-25 elicits innate lymphoid type 2 and type II NKT cells that regulate obesity in mice. J. Immunol. 191, 5349–5353 (2013).

    Article  CAS  Google Scholar 

  69. Molofsky, A. B. et al. Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages. J. Exp. Med. 210, 535–549 (2013).

    Article  CAS  Google Scholar 

  70. Qiu, Y. et al. Eosinophils and type 2 cytokine signaling in macrophages orchestrate development of functional beige fat. Cell 157, 1292–1308 (2014).

    Article  CAS  Google Scholar 

  71. Brestoff, J. R. et al. Group 2 innate lymphoid cells promote beiging of white adipose tissue and limit obesity. Nature 519, 242–246 (2015).

    Article  CAS  Google Scholar 

  72. Lee, M. W. et al. Activated type 2 innate lymphoid cells regulate beige fat biogenesis. Cell 160, 74–87 (2015).

    Article  CAS  Google Scholar 

  73. Nguyen, K. D. et al. Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis. Nature 480, 104–108 (2011).

    Article  CAS  Google Scholar 

  74. Fischer, K. et al. Alternatively activated macrophages do not synthesize catecholamines or contribute to adipose tissue adaptive thermogenesis. Nat. Med. 23, 623–630 (2017).

    Article  CAS  Google Scholar 

  75. Brestoff, J. R. & Artis, D. Immune regulation of metabolic homeostasis in health and disease. Cell 161, 146–160 (2015).

    Article  CAS  Google Scholar 

  76. Mahlakoiv, T. et al. Stromal cells maintain immune cell homeostasis in adipose tissue via production of interleukin-33. Sci. Immunol. https://doi.org/10.1126/sciimmunol.aax0416 (2019).

  77. Spallanzani, R. G. et al. Distinct immunocyte-promoting and adipocyte-generating stromal components coordinate adipose tissue immune and metabolic tenors. Sci. Immunol. https://doi.org/10.1126/sciimmunol.aaw3658 (2019).

  78. Klose, C. S. & Artis, D. Neuronal regulation of innate lymphoid cells. Curr. Opin. Immunol. 56, 94–99 (2019).

    Article  CAS  Google Scholar 

  79. Chu, C., Artis, D. & Chiu, I. M. Neuroimmune interactions in the tissues. Immunity 52, 464–474 (2020).

    Article  CAS  Google Scholar 

  80. Cardoso, F. et al. Neuro-mesenchymal units control ILC2 and obesity via a brain–adipose circuit. Nature 597, 410–414 (2021).

    Article  CAS  Google Scholar 

  81. Sasaki, T. et al. Innate lymphoid cells in the induction of obesity. Cell Rep. 28, 202–217 (2019).

    Article  CAS  Google Scholar 

  82. Dalmas, E. et al. Interleukin-33-activated islet-resident innate lymphoid cells promote insulin secretion through myeloid cell retinoic acid production. Immunity 47, 928–942 (2017).

    Article  CAS  Google Scholar 

  83. Newland, S. A. et al. Type 2 innate lymphoid cells control the development of atherosclerosis in mice. Nat. Commun. 8, 15781 (2017).

    Article  CAS  Google Scholar 

  84. O’Leary, C. E. et al. Bile acid-sensitive tuft cells regulate biliary neutrophil influx. Sci. Immunol. 7, eabj1080 (2022).

    Article  Google Scholar 

  85. Satoh-Takayama, N. et al. Bacteria-induced group 2 innate lymphoid cells in the stomach provide immune protection through induction of IgA. Immunity 52, 635–649 (2020).

    Article  CAS  Google Scholar 

  86. Kim, H. Y. et al. Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity. Nat. Med. 20, 54–61 (2014).

    Article  CAS  Google Scholar 

  87. Wang, X. et al. Interleukin-22 alleviates metabolic disorders and restores mucosal immunity in diabetes. Nature 514, 237–241 (2014). This paper reveals how the intesinal IL-22 pathway is disrupted in metabolic diseases and how exogenous IL-22 can be harnessed as a therapeutic strategy.

    Article  CAS  Google Scholar 

  88. Hasnain, S. Z. et al. Glycemic control in diabetes is restored by therapeutic manipulation of cytokines that regulate beta cell stress. Nat. Med. 20, 1417–1426 (2014).

    Article  CAS  Google Scholar 

  89. Hamaguchi, M. et al. Group 3 innate lymphoid cells protect steatohepatitis from high-fat-diet-induced toxicity. Front. Immunol. 12, 648754 (2021).

    Article  CAS  Google Scholar 

  90. Mao, K. et al. Innate and adaptive lymphocytes sequentially shape the gut microbiota and lipid metabolism. Nature 554, 255–259 (2018). This paper reveals how dynamic cross-talk between innate and adaptive lymphocytes shapes responses to microbiota, and lipid uptake or metabolism.

    Article  CAS  Google Scholar 

  91. Lio, C. J. & Huang, S. C. Circles of life: linking metabolic and epigenetic cycles to immunity. Immunology 161, 165–174 (2020).

    Article  CAS  Google Scholar 

  92. Britt, E. C., John, S. V., Locasale, J. W. & Fan, J. Metabolic regulation of epigenetic remodeling in immune cells. Curr. Opin. Biotechnol. 63, 111–117 (2020).

    Article  CAS  Google Scholar 

  93. Phan, A. T., Goldrath, A. W. & Glass, C. K. Metabolic and epigenetic coordination of T cell and macrophage immunity. Immunity 46, 714–729 (2017).

    Article  CAS  Google Scholar 

  94. Fanucchi, S., Dominguez-Andres, J., Joosten, L. A. B., Netea, M. G. & Mhlanga, M. M. The intersection of epigenetics and metabolism in trained immunity. Immunity 54, 32–43 (2021).

    Article  CAS  Google Scholar 

  95. Netea, M. G. et al. Trained immunity: a program of innate immune memory in health and disease. Science 352, aaf1098 (2016).

    Article  Google Scholar 

  96. Arguello, R. J. et al. SCENITH: a flow cytometry-based method to functionally profile energy metabolism with single-cell resolution. Cell Metab. 32, 1063–1075 (2020).

    Article  CAS  Google Scholar 

  97. Subrahmanyam, P. B. & Maecker, H. T. CyTOF measurement of immunocompetence across major immune cell types. Curr. Protoc. Cytom. 82, 9.54.1–9.54.12 (2017).

    Google Scholar 

  98. Hartmann, F. J. et al. Single-cell metabolic profiling of human cytotoxic T cells. Nat. Biotechnol. 39, 186–197 (2021).

    Article  CAS  Google Scholar 

  99. Ganesh, S. et al. Spatially resolved 3D metabolomic profiling in tissues. Sci. Adv. https://doi.org/10.1126/sciadv.abd0957 (2021).

  100. Yuan, Z. et al. SEAM is a spatial single nuclear metabolomics method for dissecting tissue microenvironment. Nat. Methods 18, 1223–1232 (2021).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

We thank members of the laboratories of L.Z. and G.F.S. for discussions and critical reading of the paper. Research in the laboratory of L.Z. is supported by the National Natural Science Foundation of China (32270943) and sponsored by Shanghai Pujiang Program (22PJ1409700). Research in the laboratory of G.F.S. is supported by the National Institutes of Health (R01AI143842, R01AI123368, R01AI145989, U01AI095608, R21CA249274, R01AI162936 and R01CA274534), the NIAID Mucosal Immunology Studies Team (MIST), the Searle Scholars Program, the American Asthma Foundation Scholar Award, an Investigators in the Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund, a Wade F.B. Thompson/Cancer Research Institute (CRI) CLIP Investigator grant, the Meyer Cancer Center Collaborative Research Initiative, Linda and Glenn Greenberg, the Dalton Family Foundation and the Roberts Institute for Research in Inflammatory Bowel Disease. G.F.S. is a CRI Lloyd J. Old STAR.

Author information

Authors and Affiliations

  1. Shanghai Immune Therapy Institute, Shanghai Jiaotong University School of Medicine-affiliated Renji Hospital, Shanghai, China

    Lei Zhou & Qingxia Lin

  2. Joan and Sanford I. Weill Department of Medicine, Division of Gastroenterology & Hepatology, Department of Microbiology and Immunology, and the Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, Cornell University, New York, NY, USA

    Gregory F. Sonnenberg

Authors
  1. Lei Zhou
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Qingxia Lin
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Gregory F. Sonnenberg
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

L.Z. and G.F.S. conceived the concepts. L.Z., Q.L. and G.F.S. wrote the paper. L.Z. and Q.L. prepared the figures.

Corresponding authors

Correspondence to Lei Zhou or Gregory F. Sonnenberg.

Ethics declarations

Competing interests

The authors declare no competing interests.

Peer review

Peer review information

Nature Metabolism thanks Stanley Huang and the other, anonymous, reviewer(s) for their contribution to the peer review of this work. Primary Handling Editor: Isabella Samuelson, in collaboration with the Nature Metabolism team.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Zhou, L., Lin, Q. & Sonnenberg, G.F. Metabolic control of innate lymphoid cells in health and disease. Nat Metab 4, 1650–1659 (2022). https://doi.org/10.1038/s42255-022-00685-8

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/s42255-022-00685-8

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing