Notch signaling in lymphopoiesis

Freddy Radtke
2003
Article

Notch signaling regulates many cell fate decisions during development of multi-cellular organisms. Signals initiated by Notch influence a wide variety of processes that include lineage specification, cell survival and proliferation, and border formation. During development of the immune system, Notch has been shown to influence the fate of both hematopoietic stem cells (HSCs) and committed progenitors. Notch appears to play an especially important role in the development of cells that mediate acquired immunity where Notch influences multiple aspects of T and B cell development. In this review, we will focus on the potential functions of Notch signaling during lymphoid development.

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Freddy Radtke
2003
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https://infoscience.epfl.ch/record/97246?ln=fr

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Notch signaling in the immune system

Nicolas Fasnacht, Freddy Radtke

The Notch signaling pathway regulates many aspects of embryonic development, as well as differentiation processes and tissue homeostasis in multiple adult organ systems. Disregulation of Notch signaling is associated with several human disorders, including cancer. In the last decade, it became evident that Notch signaling plays important roles within the hematopoietic and immune systems. Notch plays an essential role in the development of embryonic hematopoietic stem cells and influences multiple lineage decisions of developing lymphoid and myeloid cells. Moreover, recent evidence suggests that Notch is an important modulator of T cell-mediated immune responses. In this review, we discuss Notch signaling in hematopoiesis, lymphocyte development, and function as well as in T cell acute lymphoblastic leukemia.

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Hes1 Is a Critical but Context-Dependent Mediator of Canonical Notch Signaling in Lymphocyte Development and Transformation

Christelle Dubey, Ute Koch, Freddy Radtke, Agnieszka Anna Wendorff, Silvia Wirth

Although canonical Notch signaling regulates multiple hematopoietic lineage decisions including T cell and marginal zone B cell fate specification, the downstream molecular mediators of Notch function are largely unknown. We showed here that conditional inactivation of Hes1, a well-characterized Notch target gene, in adult murine bone marrow (BM) cells severely impaired T cell development without affecting other Notch-dependent hematopoietic lineages such as marginal zone B cells. Competitive mixed BM chimeras, intrathymic transfer experiments, and in vitro culture of BM progenitors on Delta-like-expressing stromal cells further demonstrated that Hes1 is required for T cell lineage commitment, but dispensable for Notch-dependent thymocyte maturation through and beyond the beta selection checkpoint. Furthermore, our data strongly suggest that Hes1 is essential for the development and maintenance of Notch-induced T cell acute lymphoblastic leukemia. Collectively, our studies identify Hes1 as a critical but context-dependent mediator of canonical Notch signaling in the hematopoietic system.

Elsevier2010

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Mechanisms of T Cell Development and Transformation

Ute Koch, Freddy Radtke

T cells are the key mediators in cell-mediated immunity. Their development and maturation involve a complex variety of interactions with nonlymphoid cell products and receptors. Highly specialized to defend against bacterial and viral infections, T cells also mediate immune surveillance against tumor cells and react to foreign tissues. T cell progenitors originate in the bone marrow and, through a series of defined and coordinated developmental stages, enter the thymus, differentiate, undergo selection, and eventually mature into functional T cells. The steps in this process are regulated through a complex transcriptional network, specific receptor-ligand pair interactions, and sensitization to trophic factors, which mediate the homing, proliferation, survival, and differentiation of developing T cells. This review examines the processes and pathways involved in the highly orchestrated development of T cell fate specification under physiological as well as pathological conditions.

2011

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