# Magnetoelectric nanoparticles drive TAF9B+ TH2 cell expansion to alleviate inflammation

## TL;DR

Researchers developed magnetoelectric nanoparticles that expand TH2 cells to reduce inflammation in autoimmune diseases.

## Contribution

A novel biomimetic magnetoelectric nanoparticle that targets T cells and modulates immune responses via ribosome interaction.

## Key findings

- DC@CFO/BFO nanoparticles enhance TH2 cell proliferation by modulating ribosomal activity.
- Systemic administration of the nanoparticles reduces inflammation in colitis and arthritis models.
- TAF9B is essential for the nanoparticle-induced immune response.

## 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 CoFe2O4@BiFeO3 particles with dendritic cell membranes to enable selective targeting of CD4+ 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 (TH2) cell proliferation. In murine models of colitis and arthritis, both systemic administration of DC@CFO/BFO and adoptive transfer of magnetoelectricity-responsive TH2 cells attenuated inflammation and restored immune homeostasis. In contrast, these effects were abrogated in Taf9b-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.

Engineered membrane-coated magnetoelectric nanoparticles drive TH2 cell expansion to alleviate autoimmune inflammation.