Essential Role of mTORC1 in Self-Renewal of Murine Alveolar Macrophages.

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Deng, W; Yang, J; Lin, X; Shin, J; Gao, J; Zhong, X-P

Published Date

  • January 1, 2017

Published In

Volume / Issue

  • 198 / 1

Start / End Page

  • 492 - 504

PubMed ID

  • 27881705

Pubmed Central ID

  • 27881705

Electronic International Standard Serial Number (EISSN)

  • 1550-6606

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.1501845

Language

  • eng

Conference Location

  • United States