The Notch signaling pathway controls short-lived effector CD8+ T cell differentiation but is dispensable for memory generation

Following an infection, naive CD8(+) T cells expand and differentiate into two main populations of effectors: short-lived effector cells (SLECs) and memory precursor effector cells (MPECs). There is limited understanding of the molecular mechanism and cellular processes governing this cell fate. Not...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2015-06, Vol.194 (12), p.5654-5662
Main Authors: Mathieu, Mélissa, Duval, Frédéric, Daudelin, Jean-François, Labrecque, Nathalie
Format: Article
Language:English
Subjects:
Animals
CD8-Positive T-Lymphocytes - cytology
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - metabolism
Cell Differentiation - genetics
Cell Differentiation - immunology
Cytokines - biosynthesis
Gene Expression
Immunologic Memory
Listeria
Listeria - immunology
Listeriosis - immunology
Listeriosis - metabolism
Lymphocyte Activation - immunology
Mice
Mice, Knockout
Receptors, Notch - genetics
Receptors, Notch - metabolism
Signal Transduction
T-Box Domain Proteins - genetics
T-Box Domain Proteins - metabolism
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Summary:Following an infection, naive CD8(+) T cells expand and differentiate into two main populations of effectors: short-lived effector cells (SLECs) and memory precursor effector cells (MPECs). There is limited understanding of the molecular mechanism and cellular processes governing this cell fate. Notch is a key regulator of cell fate decision relevant in many immunological pathways. In this study, we add to the role of Notch in cell fate decision and demonstrate that the Notch signaling pathway controls the MPEC/SLEC differentiation choice following both Listeria infection and dendritic cell immunization of mice. Although fewer SLECs were generated, Notch deficiency did not alter the rate of memory CD8(+) T cell generation. Moreover, we reveal that the Notch signaling pathway plays a context-dependent role for optimal cytokine production by effector CD8(+) T cells. Together, our results unravel critical functions for the Notch signaling pathway during effector CD8(+) T cell differentiation.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1402837