Academic Journal
Dichotomous metabolic networks govern human ILC2 proliferation and function
| العنوان: | Dichotomous metabolic networks govern human ILC2 proliferation and function |
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| المؤلفون: | Surace L., Doisne J. -M., Croft C. A., Thaller A., Escoll P., Marie S., Petrosemoli N., Guillemot V., Dardalhon V., Topazio D., Cama A., Buchrieser C., Taylor N., Amit I., Musumeci O., Di Santo J. P. |
| المساهمون: | Surace, L., Doisne, J. -M., Croft, C. A., Thaller, A., Escoll, P., Marie, S., Petrosemoli, N., Guillemot, V., Dardalhon, V., Topazio, D., Cama, A., Buchrieser, C., Taylor, N., Amit, I., Musumeci, O., Di Santo, J. P. |
| بيانات النشر: | Nature Research |
| سنة النشر: | 2021 |
| المجموعة: | Università degli Studi di Messina: IRIS |
| مصطلحات موضوعية: | Amino Acids Branched-Chain, Arginine, Case-Control Studies, Cell Proliferation, Cells Cultured, Cytokines, Energy Metabolism, Humans, Immunity Innate, Interleukin-33, Lymphocyte Activation, Mitochondria, Mitochondrial Diseases, Phenotype, Th2 Cells |
| الوصف: | Group 2 innate lymphoid cells (ILC2s) represent innate homologs of type 2 helper T cells (TH2) that participate in immune defense and tissue homeostasis through production of type 2 cytokines. While T lymphocytes metabolically adapt to microenvironmental changes, knowledge of human ILC2 metabolism is limited, and its key regulators are unknown. Here, we show that circulating ‘naive’ ILC2s have an unexpected metabolic profile with a higher level of oxidative phosphorylation (OXPHOS) than natural killer (NK) cells. Accordingly, ILC2s are severely reduced in individuals with mitochondrial disease (MD) and impaired OXPHOS. Metabolomic and nutrient receptor analysis revealed ILC2 uptake of amino acids to sustain OXPHOS at steady state. Following activation with interleukin-33 (IL-33), ILC2s became highly proliferative, relying on glycolysis and mammalian target of rapamycin (mTOR) to produce IL-13 while continuing to fuel OXPHOS with amino acids to maintain cellular fitness and proliferation. Our results suggest that proliferation and function are metabolically uncoupled in human ILC2s, offering new strategies to target ILC2s in disease settings. |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | STAMPA |
| اللغة: | English |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/34686862; info:eu-repo/semantics/altIdentifier/wos/WOS:000710077900001; volume:22; issue:11; firstpage:1367; lastpage:1374; numberofpages:8; journal:NATURE IMMUNOLOGY; https://hdl.handle.net/11570/3218642 |
| DOI: | 10.1038/s41590-021-01043-8 |
| الاتاحة: | https://hdl.handle.net/11570/3218642 https://doi.org/10.1038/s41590-021-01043-8 https://www.nature.com/articles/s41590-021-01043-8 |
| Rights: | info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.A66B4C55 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1038/s41590-021-01043-8 |
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