Publikation
Lack of conventional dendritic cells is compatible with normal development and T cell homeostasis, but causes myeloid proliferative syndrome
Wissenschaftlicher Artikel/Review - 01.12.2008
Birnberg Tal, Reizis Boris, Riethmacher Dieter, Brockschnieder Damian, Ludewig Burkhard, Brenner Ori, Krauthgamer Rita, Makia Divine, Cervantes-Barragan Luisa, Caton Michele L, Sapoznikov Anita, Bar-On Liat, Jung Steffen
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Dendritic cells are critically involved in the promotion and regulation of T cell responses. Here, we report a mouse strain that lacks conventional CD11c(hi) dendritic cells (cDCs) because of constitutive cell-type specific expression of a suicide gene. As expected, cDC-less mice failed to mount effective T cell responses resulting in impaired viral clearance. In contrast, neither thymic negative selection nor T regulatory cell generation or T cell homeostasis were markedly affected. Unexpectedly, cDC-less mice developed a progressive myeloproliferative disorder characterized by prominent extramedullary hematopoiesis and increased serum amounts of the cytokine Flt3 ligand. Our data identify a critical role of cDCs in the control of steady-state hematopoiesis, revealing a feedback loop that links peripheral cDCs to myelogenesis through soluble growth factors, such as Flt3 ligand.