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Cellular metabolic requirements associated with this transition remain poorly understood. To address this, we compared the response of lymphoid tissue (LT) Th2 cells from helminth parasite-infected mice to stimulation by IL-33 versus through the T cell receptor via anti-CD3\/CD28. We found that IL-33, but not anti-CD3\/CD28, induced the development of tissue-resident like Th2 cells expressing ST2. This was associated with IL-33 induced changes in arginine metabolism linked to mTORC1 activation and polyamine synthesis, which were required for the development of tissue-resident like Th2 cells. Furthermore, IL-33 induced transcriptional changes in genes involved in chemotaxis and cell adhesion that may be critical for tissue integration. Our findings provide insights into adaptations of Th2 cells responding to tissue-integration cues and more broadly support the view that IL-33 promotes the expression of the transcriptional program associated with tissue residency of GATA3-expressing cells in adipose and possibly other tissues.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag028","type":"journal-article","created":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T02:30:12Z","timestamp":1776306612000},"source":"Crossref","is-referenced-by-count":1,"title":["IL-33 promotes transcriptional and metabolic adaptations of tissue-resident Th2 cells"],"prefix":"10.1093","volume":"215","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5819-5694","authenticated-orcid":false,"given":"Anna K","family":"Kania","sequence":"first","affiliation":[{"name":"Department of Oncology, Bloomberg Kimmel Institute of Cancer Immunotherapy, Johns Hopkins University School of Medicine , Baltimore, MD,","place":["United 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