Journal
CELLULAR & MOLECULAR IMMUNOLOGY
Volume 16, Issue 9, Pages 757-769Publisher
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/s41423-018-0185-x
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Funding
- Program of Science and Technology Commission of Shanghai Municipality [31470845, 81430033, 31422020, 31600704, 13JC1404700]
- Ministry of Science and Technology of China [2014CB943600]
- Chinese Mega Project on Infectious Diseases
- Shu Guang project of Shanghai Municipal Education Commission [2018ZX10302301]
- Shanghai Education Development Foundation
- Brown-Cox Fellowship from Yale University
- Leukemia
- Lymphoma
- [PR093728]
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Proper control of B cell growth and metabolism is crucial for B-cell-mediated immunity, but the underlying molecular mechanisms remain incompletely understood. In this study, Sin1, a key component of mTOR complex 2 (mTORC2), specifically regulates B cell growth and metabolism. Genetic ablation of Sin1 in B cells reduces the cell size at either the transitional stage or upon antigen stimulation and severely impairs metabolism. Sin1 deficiency also severely impairs B-cell proliferation, antibody responses, and antiviral immunity. At the molecular level, Sin1 controls the expression and stability of the c-Myc protein and maintains the activity of mTORC1 through the Akt-dependent inactivation of GSK3 and TSC1/2, respectively. Therefore, our study reveals a novel and specific role for Sin1 in coordinating the activation of mTORC2 and mTORC1 to control B cell growth and metabolism.
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