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Updated: Apr 12, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
The Notch signaling pathway controls short-lived effector CD8+ T cell differentiation but is dispensable for memory
Mélissa Mathieu1, Frédéric Duval1, Jean-François Daudelin2
1Maisonneuve-Rosemont Hospital Research Center, Montreal, Quebec H1T 2M4, Canada; Department of Microbiology, Infectiology and Immunology, University of Montreal, Montreal, Quebec H3T 1J4, Canada; and.
Abstract:
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.
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