The Development of Murine Plasmacytoid Dendritic Cell Precursors Is Differentially Regulated by FLT3-ligand and Granulocyte/Macrophage Colony-Stimulating Factor

Gilliet, Michel; Boonstra, André; Paturel, Carine; Антоненко, Светлана; Xu, Xiu Ling; Trinchieri, Giorgio; O’Garra, Anne; Liu, Yong Jun

doi:10.1084/jem.20020045

Cited by 460 publications

(440 citation statements)

References 30 publications

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“…This anatomical localization and cell surface antigen expression on pDC suggest that pDC migrate from the blood to the lymph nodes through HEV in an L-selectin-dependent manner [47][48][49]. However, it has been reported that CCR7 expression is up-regulated on pDC in response to pathogenic stimuli, and that pDC migrate to the CCR7 ligands CCL19 and CCL21 expressed by stromal cells in the T cell zone and in HEV [29,50,51]. Moreover, TLR signals or type I IFN affect pDC migration via CXCR3L and CCR7 ligand induction [16,17].…”

Section: Validation Of Pdc Conversion Into Cdcmentioning

confidence: 83%

Type I interferon regulates pDC maturation and Ly49Q expression

Toma-Hirano

Namiki²,

Miyatake

et al. 2007

Eur J Immunol

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Ly49Q is expressed on peripheral mouse plasmacytoid dendritic cells (pDC). Immature Ly49Q-negative pDC precursors acquire Ly49Q in the bone marrow and then migrate into the periphery. While searching for molecules that regulate pDC maturation, we found that type I interferon (IFN) inhibited Ly49Q acquisition in vitro. Infections that induce type I IFN production by cells other than pDC (a condition mimicked by poly(I:C) injection in vivo) increase the prevalence of Ly49Q -pDC in the bone marrow and peripheral lymphoid organs in wild-type but not IFN-a/b receptor knockout BALB/c mice. Moreover, in vivo exposure to type I IFN causes some Ly49Q -, but not Ly49Q + , pDC to convert to conventional DC, defined as B220 -CD11c + CD11b + cells. These data suggest that type I IFN regulates pDC development and affects their distribution in the body.

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Section: Validation Of Pdc Conversion Into Cdcmentioning

confidence: 83%

Type I interferon regulates pDC maturation and Ly49Q expression

Toma-Hirano

Namiki²,

Miyatake

et al. 2007

Eur J Immunol

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“…Various populations of DCs and macrophages were expanded in vitro from bone marrow (BM) cells cultured in either FL, GM-CSF, or macrophage colony stimulating factor (M-CSF) as previously described (7,18). Briefly, BM was flushed from the femur and tibia of experimental mice with complete RPMI medium ([CM] 10% fetal calf serum [FCS], 2 mM L-glutamine, 10 mM HEPES, 100 U/ml penicillin, 100 g/ml streptomycin, 10 M 2-mercaptoethanol [2-ME]).…”

Section: Methodsmentioning

confidence: 99%

Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity

Lousberg

Fraser

Tovey

et al. 2010

J Virol

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“…Singlecell suspensions were prepared from thymus and spleen and were analyzed as described previously [14,26]. Dead cells were excluded by staining with PI or 7-amino-actinomycin D (7-AAD).…”

Section: Flowcytometric Analysismentioning

confidence: 99%

Oncostatin M deficiency leads to thymic hypoplasia, accumulation of apoptotic thymocytes and glomerulonephritis

et al. 2009

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Oncostatin M (OSM) has been implicated in immune regulation, though its precise role remains elusive. Here we show that OSM plays a crucial role in the prevention of autoimmune diseases. OSM-deficient mice showed normal development of T cells, B cells and DC; however, their thymus showed hypoplasia and altered medullary structure. Autoantibodies against dsDNA accumulated and glomerulonephritis developed in aged OSMdeficient mice. Apoptotic cells accumulated in the thymus of OSM-deficient mice, and the administration of dexamethasone in young OSM-deficient mice resulted in the massive accumulation of apoptotic thymocytes and production of autoantibodies. These results suggest that OSM plays a key role in the prevention of autoimmune disease by regulating the clearance of apoptotic thymocytes.Key words: Apoptosis . Autoimmunity . Phagocytosis Supporting Information available online IntroductionOncostatin M (OSM) is a member of the IL-6 family of cytokines, and the OSM receptor (OSMR) consists of gp130 and the OSMRb subunit [1]. OSM is produced by a variety of cells including hematopoietic cells and fibroblasts, and is involved in various biological systems [2]. We showed previously that the lack of OSM signaling causes altered bone marrow microenvironment [3,4]. As OSM is also produced by Th1 cells and DC [5][6][7][8], OSM is suggested to play a role in immune reactions. In fact, OSM from activated DC regulates CCL21 expression in microvascular endothelial cells and promotes the trafficking of DC to LN [8].Moreover, Tg mice that express OSM using the lck proximal promoter exhibit thymic hypertrophy [9,10], suggesting that OSM may play a role in T-cell development within the thymic environment.Apoptosis is an essential process for development and homeostasis and defective clearance of apoptotic cells can lead to production of autoantibody by releasing cell debris, breaking peripheral tolerance. Macrophages in various tissues play an essential role in the elimination of apoptotic cells by phagocytosis. A vast majority of thymocytes are depleted by apoptosis during T-cell selections; however, apoptotic cells are barely detected in the thymus, indicating the presence of a mechanism to eliminate apoptotic thymocytes. Dying cells are normally removed rapidly from tissues by phagocytes, without eliciting inflammatory or immune responses. Clearance of apoptotic cells is crucial for prevention of autoimmune diseases [11,12] 1664with impaired macrophage phagocytosis exhibit splenomegaly due to accumulation of massive quantities of apoptotic cells and such defect in humans leads to retinitis pigmentosa [13].Previously, we demonstrated that OSM induces the development of thymic macrophages with strong phagocytic activity from intrathymic progenitors via OSM-responsive thymic epithelial cells (TEC) [14,15]. In this report, we show that OSM deficiency resulted in thymic hypoplasia, defective clearance of apoptotic thymocytes, accumulation of autoantibody and glomerulonephritis. Administration of dexamethasone (Dex) in OSM-defi...

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The Development of Murine Plasmacytoid Dendritic Cell Precursors Is Differentially Regulated by FLT3-ligand and Granulocyte/Macrophage Colony-Stimulating Factor

Cited by 460 publications

References 30 publications

Type I interferon regulates pDC maturation and Ly49Q expression

Type I interferon regulates pDC maturation and Ly49Q expression

Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity

Oncostatin M deficiency leads to thymic hypoplasia, accumulation of apoptotic thymocytes and glomerulonephritis

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