Scholarlink

<p>The choroid plexus forms a key barrier and signaling interface between the brain and peripheral circulation, yet its immune landscape remains incompletely understood. Using single-cell transcriptomics combined with lineage and spatial tracing methods, we identified three biologically distinct populations of choroid plexus macrophages, defined by differential expression of CD163, MHCII or CD9. These subsets arise from separate hematopoietic waves, occupy distinct anatomical niches and differentially rely on CSF1 and IL-34 for survival. We found that TGFβ signaling is essential to maintain their tissue-specific identities, and deletion of <i>Tgfbr2</i> in these cells induces broad phenotypic reprogramming. During neuroinflammation, choroid plexus macrophages mount type I interferon responses and secrete chemokines that recruit CD8<sup>+</sup> T cells. Finally, analysis of human choroid plexus reveals macrophage subsets corresponding to those found in mice, indicating evolutionary conservation of their molecular and immune features. Together, these findings define the developmental origin, niche specialization and immune dynamics of choroid plexus macrophages.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Diversity and immune dynamics of choroid plexus macrophages are shaped by distinct developmental origins

  • 期刊论文

  • 发表日期：

    2026年1月21日

查看全文
  • Siling Du,
  • Khai M. Nguyen,
  • Alina Ulezko Antonova,
  • Jose L. Fachi,
  • Patrick Fernandes Rodrigues,
  • Alice Verdiani,
  • Martina Molgora,
  • Igor Smirnov,
  • Jasmin Herz,
  • Tornike Mamuladze,
  • Jennifer Ponce,
  • Amanda Swain,
  • Mattia Bugatti,
  • Susan Gilfillan,
  • Marina Cella,
  • William Vermi,
  • Jonathan Kipnis,
  • Marco Colonna,
  • Simone Brioschi

摘要

The choroid plexus forms a key barrier and signaling interface between the brain and peripheral circulation, yet its immune landscape remains incompletely understood. Using single-cell transcriptomics combined with lineage and spatial tracing methods, we identified three biologically distinct populations of choroid plexus macrophages, defined by differential expression of CD163, MHCII or CD9. These subsets arise from separate hematopoietic waves, occupy distinct anatomical niches and differentially rely on CSF1 and IL-34 for survival. We found that TGFβ signaling is essential to maintain their tissue-specific identities, and deletion of Tgfbr2 in these cells induces broad phenotypic reprogramming. During neuroinflammation, choroid plexus macrophages mount type I interferon responses and secrete chemokines that recruit CD8+ T cells. Finally, analysis of human choroid plexus reveals macrophage subsets corresponding to those found in mice, indicating evolutionary conservation of their molecular and immune features. Together, these findings define the developmental origin, niche specialization and immune dynamics of choroid plexus macrophages.