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Slc44a2 deficiency unveils an IFN-I–dependent feedback control of pDC egress

ABSTRACT: This project aims to characterize the proteomic landscape of bone marrow-derived plasmacytoid dendritic cells (pDCs) from wild-type (WT) and Slc44a2-deficient (cKO) mice.

ORGANISM(S): Mus Musculus

SUBMITTER: Ligong Chen

PROVIDER: PXD076360 | iProX | Tue Mar 31 00:00:00 GMT+01:00 2026

REPOSITORIES: iProX

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Slc44a2 Deficiency Unveils an IFN-I-Dependent Feedback Control of pDC Egress.

Chen Ruiqun R Wu Tao T Shi Zhen Z Verma Ravi Kumar RK Sheng Linlin L Tao Lei L Yang Mingming M Wang Yuchen Y Zhang Conggang C Fan Hao H Wu Li L Chen Ligong L

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 20260626

Plasmacytoid dendritic cells (pDCs) are a specialized subset of innate immune cells capable of sensing viral nucleic acids and rapidly producing large amounts of type I interferons (IFN-I). However, excessive IFN-I production can cause various immunopathogenic conditions. The capacity for IFN-I production by pDCs is tightly regulated, yet the underlying mechanisms remain incompletely understood. Here, we describe two levels of negative regulatory mechanisms controlling IFN-I production by pDCs. ...[more]

PMID: 42360155

Similar Datasets

Slc44a2 deficiency unveils an IFN-I–dependent feedback control of pDC egress

Project description:Plasmacytoid dendritic cells (pDCs) are a specialized subset of innate immune cells capable of sensing viral nucleic acids and rapidly producing large amounts of type I interferons (IFN-I). However, excessive IFN-I production can cause various immunopathogenic conditions. The capacity for IFN-I production by pDCs is tightly regulated, yet the underlying mechanisms remain incompletely understood. Here, we describe two levels of negative regulatory mechanisms controlling IFN-I production by pDCs. First, we identified SLC44A2 as a negative regulator of IFN-I production. SLC44A2 was highly expressed in resting pDCs but significantly downregulated upon activation. Deficiency of SLC44A2 led to excessive IFN-I production. Mechanistically, SLC44A2 may restrict IFN-I production by exporting threonine, asparagine, and glutamine, amino acids that we found to be essential for IFN-I production in pDCs. Second, we uncovered an IFN-I-dependent negative feedback mechanism controlling pDC egress. Excessive IFN-I restrained pDC migration by downregulating CCR2 and CCR5. This feedback was generally observed during viral infections, autoimmune diseases, and in Slc44a2-deficient mice. Taken together, these two regulatory mechanisms are essential for maintaining pDC homeostasis and preventing systemic overactivation of IFN-I responses.

2026-07-15 | GSE326459 | GEO

Slc44a2 deficiency unveils an IFN-I–dependent feedback control of pDC egress II

2026-07-15 | GSE326463 | GEO

The role of CD11c in dendritic cells

Project description:We cultured bone marrow derived dendritic cells from WT and CD11c KO mice. Then, a group of bone marrow dendritic cells were stimulated with LPS overnight. We obtained bone marrow derived dendritic cells with or without LPS stimulation and analyzed proteomics profiles.

2024-01-26 | PXD048907 |

RhoA ko BMDC - Control of Homeostasis and Dendritic Cell Survival by the GTPase RhoA

Project description:Differential protein expression between RhoA ko and wt bone marrow-derived dendritic cells

2015-10-01 | PXD001636 | Pride

Tec kinase deficiency in macrophages

Project description:Previous work has shown conflicting roles for Tec family kinases in regulation of Toll-like receptor (TLR)-dependent signalling in myeloid cells. In the present study, we performed a detailed investigation of the role of Btk and Tec kinases in regulating TLR signalling in several types of primary murine macrophages. We demonstrate that primary resident peritoneal macrophages deficient for Btk and Tec secrete less pro-inflammatory cytokines in response to TLR stimulation than wild type cells. In contrast, we found that bone marrow-derived and thioglycollate-elicited peritoneal macrophages deficient for Btk and Tec secrete more pro-inflammatory cytokines than wild type cells. We then compared the phosphoproteome regulated by Tec kinases and lipopolysaccharide in primary peritoneal and bone marrow derived macrophages. From this analysis we determined that Tec kinases regulate different signalling programs in these cell types. In additional studies using bone marrow-derived macrophages, we find that Tec and Btk promote phosphorylation events necessary for immunoreceptor-mediated inhibition of TLR signalling. Taken together, our results are consistent with a model where Tec kinases (Btk, Tec, Bmx) are required for TLR-dependent signalling in many types of myeloid cells. However, our data also support a cell type-specific TLR-inhibitory role for Btk and Tec that is mediated by immunoreceptor activation and signalling via PI3K.

2018-10-24 | PXD002031 | Pride

p16INK4a-deficiency promotes macrophages from classical to alternative activation

Project description:murine p16ink4a deficient (p16ko) and control (p16wt) bone marrow cells were either differentiated with normal LCM-supplemented differentiation medium to obtain bone marrow derived macrophages (BMDM) or supplemented with Interleukin 4 during differeniation to obtain M2 polarized p16wt and p16ko BMDM.

2011-07-01 | E-MEXP-3216 | biostudies-arrayexpress

Control of RelB during dendritic cell activation integrates canonical and non-canonical NFkB pathways

Project description:Dendritic cells (DC) play central roles in coordinating appropriate immune responses to pathogens. In the present study, the genes regulated by NFkB activators, RelB and cRel, in PAMP-induced bone marrow dendritic cells (BMDCs) activation was examined. Total RNA extracted from WT, relb-/-, crel-/-relb-/- bone marrow derived dendritic cells (BMDCs) were subjected to stimulation with CpG or Pam3CSK4.

2012-10-01 | E-GEOD-34990 | biostudies-arrayexpress

Effect of LPS or IFN-beta activation on gene expression of bone marrow-derived dendritic cells

Project description:To examine the changes in genes encoding proteins of metabolic pathways induced by LPS or IFN-beta in bone marrow-derived dendritic cells.

2022-05-29 | GSE204955 | GEO

Expression in IFN-gamma treated control and Atg5-/- macrophages

Project description:Type-I (α/β) and -II (γ) interferons (IFN), through an incompletely understood combination of redundant and unique mechanisms, are essential for host resistance to viral infection. We report a requirement for the Atg5-Atg12/Atg16L1 autophagosome elongation complex in IFNγ-mediated control of murine norovirus in macrophages. We use microarrays to compare transcriptional changes induced in control and Atg5 deficient macrophages by IFNγ treatment. Bone marrow derived macrophages were generated from Atg5flox/flox and Atg5flox/flox+LysM cre mice and treated with media alone or 100U/ml of IFNγ for 14 hrs. RNA was extracted using Trizol (Invitrogen) and 10 µg of RNA hybridized to Affymetrix microarrays.

2012-01-05 | E-GEOD-34863 | biostudies-arrayexpress

RNA-Seq Analysis of FACS-sorted GFP-expressing and skeletal stem cells (SSC) from the bone marrow of mice with S1P ablation in the Osterix (Osx)-lineage (Cko)

Project description:Comparison of the transcriptome of GFP-expressing cells from the bone marrow compartment of Cko mice with the transcriptome of skeletal stem cells (SSC) from the bone marrow compartment of Cko and WT mice (homozygous floxed S1P mice).

2020-06-04 | GSE146304 | GEO

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