Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

IL-33 promotes transcriptional and metabolic adaptations of tissue-resident Th2 cells

Kania AK., Sanin DE., Gu X., Gidley M., Kokosinski E., Smith A.

Animal Study, published in J Immunol (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
J Immunol (2026)
Reported sample size
—
Source database
Europe PMC
PMID
41986877
PMCID
PMC13082907
DOI
10.1093/jimmun/vkag028

Abstract (original English)

The polarization of naive CD4+ T cells into Th2 cells is initiated in lymphoid organs and completed as the cells become tissue resident, where they express ST2, the receptor for the alarmin interleukin (IL)-33, which may be a key signal for tissue integration. 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.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Lymphoid TissueTh2 CellsAnimalsMice, Inbred C57BLMiceTranscription, GeneticInterleukin-33Interleukin-1 Receptor-Like 1 Protein

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