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<p>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.</p>

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月19日

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  • Yuan Zhang,
  • Minzi Ju,
  • Suzhen Chen,
  • Wendi Yang,
  • Yang Cai,
  • Xiaoyu Yu,
  • Gang Chen,
  • Zhongxia Shen,
  • Ying Bai,
  • Hui Ren,
  • Yinghui Li,
  • Ling Shen,
  • Junxu Li,
  • Peng Shi,
  • Yonggui Yuan,
  • Bing Han,
  • Honghong Yao

摘要

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+ T (TSCM) cells, is elevated in patients and stress-susceptible mice. CD8+ TSCM cells from patients display unique transcriptional programs and correlated with depression severity. Adoptive transfer of stress-derived CD8⁺ TSCM cells induced depressive-like behavior and neuroinflammation in recipients, without brain migration. Employing a whole-body immunolabeling technology, we discover CD8+ TSCM cells migrated to intestine via the interaction of pro-platelet basic protein and C-X-C motif chemokine receptor 2. CD8+ TSCM 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+ TSCM cells and gut microbial metabolism, shedding light on potential mechanisms underlying depression and suggesting avenues for therapeutic intervention.