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Lack of conventional dendritic cells is compatible with normal development and T cell homeostasis, but causes myeloid proliferative syndrome

Lack of conventional dendritic cells is compatible with normal development and T cell homeostasis, but causes myeloid proliferative syndrome
Lack of conventional dendritic cells is compatible with normal development and T cell homeostasis, but causes myeloid proliferative syndrome
Dendritic cells are critically involved in the promotion and regulation of Tcell responses. Here, we report a mouse strain that lacks conventional CD11chi dendritic cells (cDCs) because of constitutive cell-type specific expression of a suicide gene. As expected, cDC-less mice failed to mount effective Tcell responses resulting in impaired viral clearance. In contrast, neither thymic negative selection nor T regulatory cell generation or Tcell 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.
molimmuno
1097-4180
986-997
Birnberg, Tal
261986f2-dfdc-4047-a8b9-e18d176b59ba
Bar-On, Liat
1d51775d-ecd5-4a11-be39-65b014a80ade
Sapoznikov, Anita
3634a234-25cb-418e-9ad1-156ad25a5f85
Caton, Michele L.
bdcdd335-3df9-42f4-8c4c-da7259901370
Cervantes-Barragán, Luisa
cf9995e3-1eb1-4bea-bb8f-3f4bee918a03
Makia, Divine
81f77e05-c6e2-44e8-8d42-d311ac69bec4
Krautgamer, Rita
f2c7a9ab-08ed-4a78-925f-303280fd5e47
Brenner, Ori
90db3ea0-07fd-43bc-a541-3815b9167bec
Ludewig, Burkhard
8cc0c801-f583-442e-aff5-360d478dae10
Brockschnieder, Damian
fc5b07e0-7c18-4084-ba59-b10f8ba045ef
Riethmacher, Dieter
1a0a0c2e-e94d-4d0a-a890-90107a2545bc
Reizis, Boris
4b5bcc08-108b-47b6-963c-2d6d0eb8a676
Jung, Steffan
98e30221-b869-49cd-a55b-a3c3dfb5ba3b
Birnberg, Tal
261986f2-dfdc-4047-a8b9-e18d176b59ba
Bar-On, Liat
1d51775d-ecd5-4a11-be39-65b014a80ade
Sapoznikov, Anita
3634a234-25cb-418e-9ad1-156ad25a5f85
Caton, Michele L.
bdcdd335-3df9-42f4-8c4c-da7259901370
Cervantes-Barragán, Luisa
cf9995e3-1eb1-4bea-bb8f-3f4bee918a03
Makia, Divine
81f77e05-c6e2-44e8-8d42-d311ac69bec4
Krautgamer, Rita
f2c7a9ab-08ed-4a78-925f-303280fd5e47
Brenner, Ori
90db3ea0-07fd-43bc-a541-3815b9167bec
Ludewig, Burkhard
8cc0c801-f583-442e-aff5-360d478dae10
Brockschnieder, Damian
fc5b07e0-7c18-4084-ba59-b10f8ba045ef
Riethmacher, Dieter
1a0a0c2e-e94d-4d0a-a890-90107a2545bc
Reizis, Boris
4b5bcc08-108b-47b6-963c-2d6d0eb8a676
Jung, Steffan
98e30221-b869-49cd-a55b-a3c3dfb5ba3b

Birnberg, Tal, Bar-On, Liat, Sapoznikov, Anita, Caton, Michele L., Cervantes-Barragán, Luisa, Makia, Divine, Krautgamer, Rita, Brenner, Ori, Ludewig, Burkhard, Brockschnieder, Damian, Riethmacher, Dieter, Reizis, Boris and Jung, Steffan (2008) Lack of conventional dendritic cells is compatible with normal development and T cell homeostasis, but causes myeloid proliferative syndrome. Immunity, 29 (6), 986-997. (doi:10.1016/j.immuni.2008.10.012). (PMID:19062318)

Record type: Article

Abstract

Dendritic cells are critically involved in the promotion and regulation of Tcell responses. Here, we report a mouse strain that lacks conventional CD11chi dendritic cells (cDCs) because of constitutive cell-type specific expression of a suicide gene. As expected, cDC-less mice failed to mount effective Tcell responses resulting in impaired viral clearance. In contrast, neither thymic negative selection nor T regulatory cell generation or Tcell 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.

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Published date: 19 December 2008
Keywords: molimmuno
Organisations: Human Genetics

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Local EPrints ID: 66667
URI: https://eprints.soton.ac.uk/id/eprint/66667
ISSN: 1097-4180
PURE UUID: 30b6a011-d183-4018-a311-e5cabec45763

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Date deposited: 07 Jul 2009
Last modified: 19 Jul 2017 00:23

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Contributors

Author: Tal Birnberg
Author: Liat Bar-On
Author: Anita Sapoznikov
Author: Michele L. Caton
Author: Luisa Cervantes-Barragán
Author: Divine Makia
Author: Rita Krautgamer
Author: Ori Brenner
Author: Burkhard Ludewig
Author: Damian Brockschnieder
Author: Boris Reizis
Author: Steffan Jung

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