Essential Role of mTORC1 in Self-Renewal of Murine Alveolar Macrophages
In: The Journal of Immunology, Jg. 198 (2017), S. 492-504
Online
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Zugriff:
Alveolar macrophages (AMϕ) have the capacity of local self-renewal through adult life; however, mechanisms that regulate AMϕ self-renewal remain poorly understood. We found that myeloid-specific deletion of Raptor, an essential component of the mammalian/mechanistic target of rapamycin complex (mTORC)1, resulted in a marked decrease of this population of cells accompanying altered phenotypic features and impaired phagocytosis activity. We demonstrated further that Raptor/mTORC1 deficiency did not affect AMϕ development, but compromised its proliferative activity at cell cycle entry in the steady-state as well as in the context of repopulation in irradiation chimeras. Mechanically, mTORC1 confers AMϕ optimal responsiveness to GM-CSF–induced proliferation. Thus, our results demonstrate an essential role of mTORC1 for AMϕ homeostasis by regulating proliferative renewal.
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Essential Role of mTORC1 in Self-Renewal of Murine Alveolar Macrophages
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Autor/in / Beteiligte Person: | Lin, Xingguang ; Zhong, Xiao-Ping ; Gao, Jimin ; Shin, Jinwook ; Deng, Wenhai ; Yang, Jialong |
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Zeitschrift: | The Journal of Immunology, Jg. 198 (2017), S. 492-504 |
Veröffentlichung: | The American Association of Immunologists, 2017 |
Medientyp: | unknown |
ISSN: | 1550-6606 (print) ; 0022-1767 (print) |
DOI: | 10.4049/jimmunol.1501845 |
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