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CSF1R regulates the dendritic cell pool size in adult mice via embryo-derived tissue-resident macrophages.


ABSTRACT: Regulatory mechanisms controlling the pool size of spleen dendritic cells (DC) remain incompletely understood. DCs are continuously replenished from hematopoietic stem cells, and FLT3-mediated signals cell-intrinsically regulate homeostatic expansion of spleen DCs. Here we show that combining FLT3 and CSF1R-deficiencies results in specific and complete abrogation of spleen DCs in vivo. Spatiotemporally controlled CSF1R depletion reveals a cell-extrinsic and non-hematopoietic mechanism for DC pool size regulation. Lack of CSF1R-mediated signals impedes the differentiation of spleen macrophages of embryonic origin, and the resulted macrophage depletion during development or in adult mice results in loss of DCs. Moreover, embryo-derived macrophages are important for the physiologic regeneration of DC after activation-induced depletion in situ. In summary, we show that the differentiation of DC and their regeneration relies on ontogenetically distinct spleen macrophages, thereby providing a novel regulatory principle that may also be important for the differentiation of other hematopoietic cell types.

SUBMITTER: Percin GI 

PROVIDER: S-EPMC6290072 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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CSF1R regulates the dendritic cell pool size in adult mice via embryo-derived tissue-resident macrophages.

Percin Gulce Itir GI   Eitler Jiri J   Kranz Andrea A   Fu Jun J   Pollard Jeffrey W JW   Naumann Ronald R   Waskow Claudia C  

Nature communications 20181211 1


Regulatory mechanisms controlling the pool size of spleen dendritic cells (DC) remain incompletely understood. DCs are continuously replenished from hematopoietic stem cells, and FLT3-mediated signals cell-intrinsically regulate homeostatic expansion of spleen DCs. Here we show that combining FLT3 and CSF1R-deficiencies results in specific and complete abrogation of spleen DCs in vivo. Spatiotemporally controlled CSF1R depletion reveals a cell-extrinsic and non-hematopoietic mechanism for DC poo  ...[more]

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