Migration of CD8 + TSCM cells into intestine via PPBP-CXCR2 axis increases host stress susceptibility by inhibiting gut microbiome-derived homovanillic acid.

Zhang, Yuan; Ju, Minzi; Chen, Suzhen; Yang, Wendi; Cai, Yang; Yu, Xiaoyu; Chen, Gang; Shen, Zhongxia et al. · Nat Commun · 2025

basic_science · Level V

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Abstract

Psychosocial stress impacts immune system and brain function, yet mechanisms linking peripheral immune dysregulation to major depressive disorder remain unclear. Here, we demonstrate that a specific subset of T cells, the stem cell-like memory CD8<sup>+</sup> T (T<sub>SCM</sub>) cells, is elevated in patients and stress-susceptible mice. CD8<sup>+</sup> T<sub>SCM</sub> cells from patients display unique transcriptional programs and correlated with depression severity. Adoptive transfer of stress-derived CD8⁺ T<sub>SCM</sub> cells induced depressive-like behavior and neuroinflammation in recipients, without brain migration. Employing a whole-body immunolabeling technology, we discover CD8<sup>+</sup> T<sub>SCM</sub> cells migrated to intestine via the interaction of pro-platelet basic protein and C-X-C motif chemokine receptor 2. CD8<sup>+</sup> T<sub>SCM</sub> cells decrease the abundance of tyrosine-metabolizing bacteria to reducing homovanillic acid production, triggered neuroinflammation and depressive symptoms. Thus, our findings uncover a complex interplay between CD8<sup>+</sup> T<sub>SCM</sub> cells and gut microbial metabolism, shedding light on potential mechanisms underlying depression and suggesting avenues for therapeutic intervention.

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