Human thymus contains IFN-α–producing CD11c–, myeloid CD11c+, and mature interdigitating dendritic cells

Bendriss‐Vermare, Nathalie; Barthélemy, Clarisse; Durand, Isabelle; Bruand, Corinne; Dezutter‐Dambuyant, Colette; Moulian, Nathalie; Berrih‐Aknin, Sonia; Caux, Christophe; Trinchieri, Giorgio; Brière, Francine

doi:10.1172/jci11734

Cited by 179 publications

(87 citation statements)

References 48 publications

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“…The first strand cDNA synthesis containing 1 g of total RNA was primed with oligo(dT). To quantify GM-CSF transcripts, the LightCycler System (Roche Applied Science) was used (28). PCRs were performed using SYBR Green I master mix and specific primers for mouse GM-CSF and mouse ␤-actin, which were designed as described previously (11,29).…”

Section: Methodsmentioning

confidence: 99%

Statins Suppress Oxidized Low Density Lipoprotein-induced Macrophage Proliferation by Inactivation of the Small G Protein-p38 MAPK Pathway

Senokuchi

Matsumura

Sakai

et al. 2005

Journal of Biological Chemistry

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Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase (statins) ameliorate atherosclerotic diseases. Macrophages play an important role in the development and subsequent stability of atherosclerotic plaques. We reported previously that oxidized low density lipoprotein (Ox-LDL) induced macrophage proliferation through the secretion of granulocyte/macrophage colony-stimulating factor (GM-CSF) and the consequent activation of p38 MAPK. The present study was designed to elucidate the mechanism of the inhibitory effect of statins on macrophage proliferation. Mouse peritoneal macrophages were used in our study. Cerivastatin and simvastatin each inhibited Ox-LDL-induced [ 3 H]thymidine incorporation into macrophages. Statins did not inhibit Ox-LDL-induced GM-CSF production, but inhibited GM-CSF-induced p38 MAPK activation. Farnesyl transferase inhibitor and geranylgeranyl transferase inhibitor inhibited GM-CSF-induced macrophage proliferation, and farnesyl pyrophosphate and geranylgeranyl pyrophosphate prevented the effect of statins. GM-CSF-induced p38 MAPK phosphorylation was also inhibited by farnesyl transferase inhibitor or geranylgeranyl transferase inhibitor, and farnesyl pyrophosphate and geranylgeranyl pyrophosphate prevented the suppression of GM-CSF-induced p38 MAPK phosphorylation by statins. Furthermore, we found that statin significantly inhibited the membrane translocation of the small G protein family members Ras and Rho. GM-CSF-induced p38 MAPK activation and macrophage proliferation was partially inhibited by overexpression of dominant negative Ras and completely by that of RhoA. In conclusion, statins inhibited GM-CSF-induced Ras-or RhoA-p38 MAPK signal cascades, thereby suppressing Ox-LDL-induced macrophage proliferation. The significant inhibition of macrophage proliferation by statins may also explain, at least in part, their anti-atherogenic action.

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Section: Methodsmentioning

confidence: 99%

Statins Suppress Oxidized Low Density Lipoprotein-induced Macrophage Proliferation by Inactivation of the Small G Protein-p38 MAPK Pathway

Senokuchi

Matsumura

Sakai

et al. 2005

Journal of Biological Chemistry

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“…For quantifying SR-A and glyceraldehyde-3-phosphate dehydrogenase transcript, the LightCycler System (Roche Applied Science) was used (32). PCRs were performed using SYBR Green I master mix and specific primer for human SR-A.…”

Section: Methodsmentioning

confidence: 99%

Expression of Class A Scavenger Receptor Is Enhanced by High Glucose in Vitro and under Diabetic Conditions in Vivo

Fukuhara-Takaki

Sakai

Sakamoto

et al. 2005

Journal of Biological Chemistry

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In the early stage of atherosclerosis, macrophages take up chemically modified low density lipoproteins (LDL) through the scavenger receptors, leading to foam cell formation in atherosclerotic lesions. To get insight into a role of the scavenger receptors in diabetes-enhanced atherosclerotic complications, the effects on class A scavenger receptor (SR-A) of high glucose exposure in vitro as well as the diabetic conditions in vivo were determined in the present study. The in vitro experiments demonstrated that high glucose exposure to human monocyte-derived macrophages led to an increased SR-A expression with a concomitant increase in the endocytic uptake of acetylated LDL and oxidized LDL. The endocytic process was significantly suppressed by an anti-SR-A neutralizing antibody. Stability analyses revealed a significant increased stability of SR-A at a mRNA level but not a protein level, indicating that high glucoseinduced up-regulation of SR-A is due largely to increased stability of SR-A mRNA. High glucose-enhanced SR-A expression was prevented by protein kinase C and NAD(P)H oxidase inhibitors as well as antioxidants. High glucose-enhanced production of intracellular peroxides was visualized in these cells, which was attenuated by an antioxidant. The in vivo experiments demonstrated that peritoneal macrophages from streptozotocin-induced diabetic mice increased SR-A expression when compared with those from nondiabetic mice. Endocytic degradation of acetylated LDL and oxidized LDL were also increased with these macrophages but not with the corresponding macrophages from diabetic SR-A knock-out mice. These in vitro and in vivo results probably suggest that reactive oxygen species generated from a protein kinase C-dependent NAD(P)H oxidase pathway plays a role in the high glucose-induced up-regulation of SR-A, leading to the increased endocytic degradation of modified LDL for foam cell formation. This could be one mechanism for an increased rate of atherosclerosis in patients with diabetes.

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“…In the steady state, the pDCs are present in the thymus and all secondary lymphoid organs (Asselin-Paturel et al, 2003;Bendriss-Vermare et al, 2001;Okada et al, 2003;Summers et al, 2001), but they are difficult to detect in most peripheral tissues (De Heer et al, 2004;Wollenberg et al, 2002). This has led to the notion that pDCs enter the spleen and LNs through the blood but not via the lymph (Randolph et al, 2008), a view supported by the apparent lack of pDCs in gut and liver afferent lymph collected from cannulated rats (Yrlid et al, 2006).…”

Section: Pdc Migration In the Steady State And In Response To Infectionmentioning

confidence: 99%

Antigen-Presentation Properties of Plasmacytoid Dendritic Cells

2008

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One of the remaining enigmas of the dendritic cell (DC) network is the potential contribution of plasmacytoid DCs (pDCs) to antigen presentation. Although the antigen-presentation capacity of conventional DCs (cDCs) is clearly defined, pDCs are generally attributed as having little, if any, antigen-presentation function. Instead, pDCs are regarded as immunomodulating cells, capable of directing the immune response through their secretion of large amounts of type I interferons. In this review, we examine the evidence for a potential role of pDC in antigen capture, processing, and presentation to T cells at sites of infection and in the lymph nodes.

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Human thymus contains IFN-α–producing CD11c–, myeloid CD11c+, and mature interdigitating dendritic cells

Cited by 179 publications

References 48 publications

Statins Suppress Oxidized Low Density Lipoprotein-induced Macrophage Proliferation by Inactivation of the Small G Protein-p38 MAPK Pathway

Statins Suppress Oxidized Low Density Lipoprotein-induced Macrophage Proliferation by Inactivation of the Small G Protein-p38 MAPK Pathway

Expression of Class A Scavenger Receptor Is Enhanced by High Glucose in Vitro and under Diabetic Conditions in Vivo

Antigen-Presentation Properties of Plasmacytoid Dendritic Cells

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