Id2 expression delineates differential checkpoints in the genetic program of CD8α+ and CD103+ dendritic cell lineages.
Jacob T. Jackson,Yifang Hu,Ruijie Liu,Frederick Masson,Angela D'Amico,Sebastian Carotta,Annie Xin,Annie Xin,Mary J Camilleri,Adele M. Mount,Axel Kallies,Axel Kallies,Li Wu,Li Wu,Gordon K. Smyth,Gordon K. Smyth,Stephen L. Nutt,Stephen L. Nutt,Gabrielle T. Belz,Gabrielle T. Belz +19 more
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TLDR
It is shown that Id2 is broadly expressed in all cDC subsets with the highest expression in CD103+ and CD8α+ lineages and that Irf‐8 and Batf3 regulate distinct stages in DC differentiation during the development of cDCs.Abstract:
Dendritic cells (DCs) have critical roles in the induction of the adaptive immune response. The transcription factors Id2, Batf3 and Irf-8 are required for many aspects of murine DC differentiation including development of CD8α+ and CD103+ DCs. How they regulate DC subset specification is not completely understood. Using an Id2-GFP reporter system, we show that Id2 is broadly expressed in all cDC subsets with the highest expression in CD103+ and CD8α+ lineages. Notably, CD103+ DCs were the only DC able to constitutively cross-present cell-associated antigens in vitro. Irf-8 deficiency affected loss of development of virtually all conventional DCs (cDCs) while Batf3 deficiency resulted in the development of Sirp-α− DCs that had impaired survival. Exposure to GM-CSF during differentiation induced expression of CD103 in Id2-GFP+ DCs. It did not restore cross-presenting capacity to Batf3−/− or CD103−Sirp-α−DCs in vitro. Thus, Irf-8 and Batf3 regulate distinct stages in DC differentiation during the development of cDCs. Genetic mapping DC subset differentiation using Id2-GFP may have broad implications in understanding the interplay of DC subsets during protective and pathological immune responses.read more
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Development of conventional dendritic cells: from common bone marrow progenitors to multiple subsets in peripheral tissues
TL;DR: This review of conventional dendritic cell development from the distinct progenitors in the bone marrow through to the distinct cDC subsets found in barrier tissues, providing an overview of the different subsets described in each location.
Journal ArticleDOI
Bcl11b is essential for group 2 innate lymphoid cell development
Jennifer A. Walker,Christopher J. Oliphant,Alexandros Englezakis,Yong Yu,Simon Clare,Hans Reimer Rodewald,Gabrielle T. Belz,Pentao Liu,Padraic G. Fallon,Andrew N. J. McKenzie +9 more
TL;DR: Mice deficient in Bcl11b exhibit a lack of ILC2 development and an expansion of RORγt+ ILC3s and are unable to clear Nippostrongylus brasiliensis worm infection, but can clear Citrobacter rodentium.
Journal ArticleDOI
Genetic models of human and mouse dendritic cell development and function.
David A. Anderson,Charles-Antoine Dutertre,Florent Ginhoux,Florent Ginhoux,Florent Ginhoux,Kenneth M. Murphy +5 more
TL;DR: Genetic models of dendritic cell (DC) development in mice have aided the understanding of the redundant and non-redundant functions of DC subsets and enabled translation of these findings to human DCs.
Journal ArticleDOI
TCF-1 Controls ILC2 and NKp46+RORγt+ Innate Lymphocyte Differentiation and Protection in Intestinal Inflammation
Lisa A. Mielke,Joanna R Groom,Lucille C. Rankin,Cyril Seillet,Frederick Masson,Tracy L Putoczki,Gabrielle T. Belz,Gabrielle T. Belz +7 more
TL;DR: It is demonstrated that T cell factor 1 (TCF-1; encoded by Tcf7), a transcription factor also important for NK and T cell differentiation, is expressed by multiple innate lymphoid cell subsets, including GATA3+ nuocytes (ILC2) and NKp46+ ILCs ( ILC3), which confer protection against lung and intestinal inflammation.
Journal ArticleDOI
Local Modulation of Antigen-Presenting Cell Development after Resolution of Pneumonia Induces Long-Term Susceptibility to Secondary Infections
Antoine Roquilly,Hamish E G McWilliam,Cédric Jacqueline,Zehua Tian,Raphaël Cinotti,Marie Rimbert,Linda M. Wakim,Irina Caminschi,Mireille H. Lahoud,Gabrielle T. Belz,Axel Kallies,Justine D. Mintern,Karim Asehnoune,Jose A Villadangos +13 more
TL;DR: Following a severe primary infection, the risk of developing pneumonia increases due to acquired immune defects collectively known as sepsis‐induced immunosuppression, and Roquilly et al. show that resolution of the primary infection changed the local environment, leading to the development of DCs and macrophages that are functionally impaired in terms of T cell activation and instead exhibit tolerogenic properties that contribute to immune suppression.
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