期刊
IMMUNITY
卷 43, 期 1, 页码 92-106出版社
CELL PRESS
DOI: 10.1016/j.immuni.2015.06.012
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资金
- Deutsche Forschungsgemeinschaft (DFG) Research Unit (FOR) [1336]
- Gemeinnutzige Hertie-Stiftung
- International Graduate School of Immunotherapy (GRK) [1043]
- Sixth Research Framework Programme of the European Union [MUGEN LSHG-CT-2005-005203]
- MRC research grant [G0801296]
- Mechanisms of the Interleukin action in neuronal injury
- [SFB/TRR128 TP A07]
- [TP B04]
- MRC [G0801296] Funding Source: UKRI
- Medical Research Council [G0801296] Funding Source: researchfish
During early embryogenesis, microglia arise from yolk sac progenitors that populate the developing central nervous system (CNS), but how the tissue-resident macrophages are maintained throughout the organism's lifespan still remains unclear. Here, we describe a system that allows specific, conditional ablation of microglia in adult mice. We found that the microglial compartment was reconstituted within 1 week of depletion. Microglia repopulation relied on CNS-resident cells, independent from bone-marrow-derived precursors. During repopulation, microglia formed clusters of highly proliferative cells that migrated apart once steady state was achieved. Proliferating microglia expressed high amounts of the interleukin-1 receptor (IL-1R), and treatment with an IL-1R antagonist during the repopulation phase impaired microglia proliferation. Hence, microglia have the potential for efficient self-renewal without the contribution of peripheral myeloid cells, and IL-1R signaling participates in this restorative proliferation process.
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