Magnetoelectric nanoparticles drive TAF9B(+) T(H)2 cell expansion to alleviate inflammation.

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(2)O(4)@BiFeO(3) 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 (T(H)2) cell proliferation. In murine models of colitis and arthritis, both systemic administration of DC@CFO/BFO and adoptive transfer of magnetoelectricity-responsive T(H)2 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.