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miR-150 Regulates Memory CD8 T Cell Differentiation via c-Myb
Zeyu Chen1, Erietta Stelekati1, Makoto Kurachi1
1Department of Microbiology, University of Pennsylvania, Philadelphia, PA, USA; Institute for Immunology, University of Pennsylvania, Philadelphia, PA, USA.
Abstract:
MicroRNAs play an important role in T cell responses. However, how microRNAs regulate CD8 T cell memory remains poorly defined. Here, we found that miR-150 negatively regulates CD8 T cell memory in vivo. Genetic deletion of miR-150 disrupted the balance between memory precursor and terminal effector CD8 T cells following acute viral infection. Moreover, miR-150-deficient memory CD8 T cells were more protective upon rechallenge. A key circuit whereby miR-150 repressed memory CD8 T cell development through the transcription factor c-Myb was identified. Without miR-150, c-Myb was upregulated and anti-apoptotic targets of c-Myb, such as Bcl-2 and Bcl-xL, were also increased, suggesting a miR-150-c-Myb survival circuit during memory CD8 T cell development. Indeed, overexpression of non-repressible c-Myb rescued the memory CD8 T cell defects caused by overexpression of miR-150. Overall, these results identify a key role for miR-150 in memory CD8 T cells through a c-Myb-controlled enhanced survival circuit.
Insights
MicroRNA 150 (miR-150) negatively regulates CD8 T cell memory. Deleting miR-150 enhances CD8 T cell memory and protection upon rechallenge by upregulating the transcription factor c-Myb.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- MicroRNAs are crucial regulators of T cell responses.
- The specific role of microRNAs in CD8 T cell memory development is not well understood.
Purpose of the Study:
- To investigate the role of microRNAs in regulating CD8 T cell memory.
- To identify the molecular mechanisms by which microRNAs control CD8 T cell memory formation.
Main Methods:
- In vivo studies involving genetic deletion of miR-150 in mice.
- Analysis of CD8 T cell populations following viral infection and rechallenge.
- Investigation of the miR-150-c-Myb regulatory axis and its downstream targets (Bcl-2, Bcl-xL).
Main Results:
- Genetic deletion of miR-150 enhanced CD8 T cell memory and protective immunity upon rechallenge.
- miR-150 was found to negatively regulate CD8 T cell memory by repressing the transcription factor c-Myb.
- Upregulation of c-Myb and its anti-apoptotic targets (Bcl-2, Bcl-xL) in miR-150-deficient CD8 T cells suggests a survival circuit.
Conclusions:
- miR-150 plays a critical inhibitory role in CD8 T cell memory development.
- The miR-150-c-Myb axis regulates CD8 T cell survival and memory formation.
- Targeting this pathway could enhance T cell-based immunotherapies.
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