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DNGR-1 regulates proliferation and migration of bone marrow dendritic cell progenitors

ABSTRACT: DNGR-1 regulates proliferation and migration of bone marrow dendritic cell progenitors

PROVIDER: PRJNA1167788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30857721_1.fastq.gz	Fastqsanger.gz
	SRR30857721_2.fastq.gz	Fastqsanger.gz
	SRR30857722_1.fastq.gz	Fastqsanger.gz
	SRR30857722_2.fastq.gz	Fastqsanger.gz
	SRR30857723_1.fastq.gz	Fastqsanger.gz

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DNGR-1 regulates proliferation and migration of bone marrow dendritic cell progenitors

Project description:Conventional dendritic cells (cDCs) are sentinel cells that play a crucial role in both innate and adaptive immune responses. cDCs originate from a common progenitor (pre-cDC) in the bone marrow (BM) that travels via the blood to seed peripheral tissues before locally differentiating into functional cDC1 and cDC2 cells, a process known as cDCpoiesis. We show that DNGR-1, an innate immune receptor expressed by cDC progenitors and type 1 cDCs, functionally regulates cDCpoiesis in mice. In a competitive chimera setting, cDC progenitors lacking DNGR-1 exhibit increased proliferation and tissue migratory potential. Compared to their wildtype counterparts, DNGR-1-deficient cDC progenitor cells display superior colonization of peripheral tissues but an altered distribution. These findings suggest that cDCpoiesis can be regulated in part by cell-intrinsic processes driven by signals from innate immune receptors such as DNGR-1 that may respond to alterations in the BM milieu

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DNGR-1 signalling limits dendritic cell activation for optimal antigen cross-presentation

Project description:Innate immune receptors often induce activation of conventional dendritic cells (cDCs) and enhance antigen (cross-)presentation, favouring immune responses. DNGR-1 (CLEC9A), a receptor expressed by type 1 cDCs (cDC1s) and implicated in immune responses to viruses and cancer, recognises F-actin exposed on dead cell remnants and promotes cross-presentation of associated antigens. Here, we show that recruitment of phosphatase SHIP1, a process governed by a single amino acid residue adjacent to the signalling motif of the receptor, partly explains how DNGR-1 fails to trigger cDC1 activation in vitro. Substituting this residue converts DNGR-1 into an activating receptor but decreases induction of cross-presentation of dead cell-associated antigens. Introducing the reverse mutation into the related receptor Dectin-1 impairs its activation capacity while enhancing its ability to promote cross-presentation. These findings reveal a functional trade-off in receptor signalling and suggest that DNGR-1 has evolved to prioritise antigen cross-presentation over cellular activation, possibly to minimise inflammatory responses to dead cells.

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Gene expression profile of CD141+DNGR-1+ dendritic cells (cDC1s) derived in vitro from multipotent lymphoid progenitors (MLP) or common myeloid progenitors (CMP)

Project description:CD141+DNGR-1+ cDC1 have a dual origin. Both MLP and CMP can differentiate in CD141+DNGR-1+ cDC1s. Using Affymetrix microarrays (GeneChip Human Gene 2.0 ST) we compared gene expression of CD141+DNGR-1+ cDC1s originating either from MLPs or CMPs

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