Magnetoelectric nanoparticles drive TAF9B<sup>+</sup> T<sub>H</sub>2 cell expansion to alleviate inflammation.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 41671377.
- Also identified by DOI 10.1126/sciadv.adz3199 and PMC identifier 12893300.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Stimuli-responsive nanomaterials represent a promising platform for immunomodulation. However, their application in orchestrating T cell responses remains limited. Here, we develop a biomimetic magnetoelectric nanoparticle (DC@CFO/BFO) by coating core-shell CoFe<sub>2</sub>O<sub>4</sub>@BiFeO<sub>3</sub> particles with dendritic cell membranes to enable selective targeting of CD4<sup>+</sup> T cells. Under magnetic field stimulation, DC@CFO/BFO localizes to ribosomes and enhances protein synthesis by modulating electrostatic interactions at the ribosomal exit tunnel. This ribosome-targeted modulation promotes type II immune response via IL-4 induction and TAF9B-dependent transcriptional programming, thereby enhancing T helper 2 (T<sub>H</sub>2) cell proliferation. In murine models of colitis and arthritis, both systemic administration of DC@CFO/BFO and adoptive transfer of magnetoelectricity-responsive T<sub>H</sub>2 cells attenuated inflammation and restored immune homeostasis. In contrast, these effects were abrogated in <i>Taf9b</i>-deficient T cells, underscoring the essential role of TAF9B in mediating this response. Collectively, our findings identify magnetoelectric nanocomposites as a potent tool for T cell engineering and highlight a translational strategy for the treatment of autoimmune inflammation.
Medical subject headings
- Th2 Cells
- Inflammation
- Nanoparticles