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A Myc-dependent division timer complements a cell-death timer to regulate T cell and B cell responses
Susanne Heinzel1,2, Tran Binh Giang1,2, Andrey Kan1,2
1Division of Immunology, The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia.
Nature Immunology
|November 8, 2016
Summary
Cell proliferation in T and B lymphocytes is controlled by timed changes in the proto-oncoprotein Myc. This intrinsic timing mechanism, coupled with a programmed cell death pathway, shapes the immune response.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- T and B lymphocytes must precisely regulate their proliferation upon activation to mount an effective immune response.
- Controlling the magnitude of lymphocyte expansion is crucial for preventing autoimmunity and ensuring pathogen clearance.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying the timed control of T and B lymphocyte proliferation.
- To investigate the role of the proto-oncoprotein Myc in regulating lymphocyte cell cycle progression and survival.
Main Methods:
- Analysis of Myc protein levels during lymphocyte activation and cell division.
- Investigating the effects of Myc overexpression on lymphocyte proliferation and survival.
- Characterizing the 'time-to-die' mechanism programmed after lymphocyte activation.
Main Results:
- Lymphocyte division cessation is triggered by a critical threshold of falling Myc levels, indicating a cell-intrinsic temporal controller.
- Overexpression of Myc does not lead to indefinite proliferation due to a separate, heritable 'time-to-die' mechanism.
- These competing intrinsic timed fates generate the characteristic pattern of lymphocyte expansion followed by cell loss.
Conclusions:
- Lymphocyte proliferation is governed by a sophisticated interplay between Myc-dependent cell-cycle control and a programmed cell death pathway.
- These cell-intrinsic temporal mechanisms dictate the canonical shape of the adaptive immune response.
- Modulations in these timed processes can significantly impact lymphocyte numbers, with implications for immune regulation and oncogenesis.
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