Immunity | 卵黄囊起源的CD163⁺巨噬细胞决定疟疾后脾脏韧性
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TL;DR - An Immunity study identifies yolk-sac-derived CD163-high red-pulp macrophages as essential for splenic recovery after malaria. Malaria-induced hemolysis permanently eliminates these cells, disrupting macrophage signaling and causing lasting damage to splenic architecture and hematopoietic recovery.
- Single-cell RNA sequencing and lineage tracing identified an iron-recycling CD163-high macrophage subset that retains its embryonic yolk-sac origin into adulthood.
- Hemolytic stress—not persistent parasites or generalized inflammation—caused this subset’s irreversible loss across multiple malaria models.
- Loss of CD163-high macrophages disrupted GDF15–TGFBR2 trophic signaling to marginal metallophilic macrophages, impairing their regeneration and destabilizing the splenic marginal zone.
- Reciprocal support from marginal-zone macrophages was also necessary for red-pulp macrophage development, iron storage, and recovery of red blood cell production.
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Immunity | 卵黄囊起源的CD163⁺巨噬细胞决定疟疾后脾脏韧性
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TL;DR - An Immunity study identifies yolk-sac-derived CD163-high red-pulp macrophages as essential for splenic recovery after malaria. Malaria-induced hemolysis permanently eliminates these cells, disrupting macrophage signaling and causing lasting damage to splenic architecture and hematopoietic recovery.
- Single-cell RNA sequencing and lineage tracing identified an iron-recycling CD163-high macrophage subset that retains its embryonic yolk-sac origin into adulthood.
- Hemolytic stress—not persistent parasites or generalized inflammation—caused this subset’s irreversible loss across multiple malaria models.
- Loss of CD163-high macrophages disrupted GDF15–TGFBR2 trophic signaling to marginal metallophilic macrophages, impairing their regeneration and destabilizing the splenic marginal zone.
- Reciprocal support from marginal-zone macrophages was also necessary for red-pulp macrophage development, iron storage, and recovery of red blood cell production.