The chemokine system: tuning and shaping by regulation of receptor expression and coupling in polarized responses

Locati, Massimo; Otero, Karel; Schioppa, Tiziana; Signorelli, Paola; Perrier, Patrick; Baviera, Stefania; Sozzani, Silvano; Mantovani, Alberto

doi:10.1034/j.1398-9995.2002.02166.x

Cited by 68 publications

(62 citation statements)

References 103 publications

(90 reference statements)

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“…Expression of chemokine receptors has been shown to be regulated by different inflammatory mediators (22). In asthma, the cytokine environment is characterized by increased TNF-␣, IL-4, and IL-13 levels (23).…”

Section: Tnf-␣ and Ifn-␥ Up-regulate The Expression Of Ccr1 By Asmcmentioning

confidence: 99%

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

Joubert

Lajoie-Kadoch

Welman

et al. 2008

The Journal of Immunology

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C-C chemokines such as CCL11, CCL5, and CCL3 are central mediators in the pathogenesis of asthma. They are mainly associated with the recruitment and the activation of specific inflammatory cells, such as eosinophils, lymphocytes, and neutrophils. It has recently been shown that they can also activate structural cells, such as airway smooth muscle and epithelial cells. The aims of this study were to examine the expression of the CCL3 receptor, CCR1, on human airway smooth muscle cells (ASMC) and to document the regulation of this receptor by cytokines involved in asthma pathogenesis. We first demonstrated that CCR1 mRNA is increased in the airways of asthmatic vs control subjects and showed for the first time that ASMC express CCR1 mRNA and protein, both in vitro and in vivo. Calcium mobilization by CCR1 ligands confirmed its functionality on ASMC. Stimulation of ASMC with TNF-α and, to a lesser extent, IFN-γ resulted in an up-regulation of CCR1 expression, which was totally suppressed by both dexamethasone or mithramycin. Taken together, our data suggest that CCR1 might be involved in the pathogenesis of asthma, through the activation of ASMC by its ligands.

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Section: Tnf-␣ and Ifn-␥ Up-regulate The Expression Of Ccr1 By Asmcmentioning

confidence: 99%

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

Joubert

Lajoie-Kadoch

Welman

et al. 2008

The Journal of Immunology

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“…The chemokine superfamily includes a large number of low molecular weight chemotactic proteins that regulate the trafficking of leukocytes to inflammatory sites [2][3][4]. Chemokines are generally 8-11 kDa in size and contain four conserved cysteine amino acid residues linked by disulfide bonds.…”

Section: Chemokines and Their Receptorsmentioning

confidence: 99%

Chemokines in tumor angiogenesis and metastasis

Singh

Sadanandam

Singh

2007

Cancer Metastasis Rev

158

132

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Chemokines are a large group of low molecular weight cytokines that are known to selectively attract and activate different cell types. Although the primary function of chemokines is well recognized as leukocyte attractants, recent evidences indicate that they also play a role in number of tumor-related processes, such as growth, angiogenesis and metastasis. Chemokines activate cells through cell surface seven trans-membranes, G-protein-coupled receptors (GPCR). The role played by chemokines and their receptors in tumor pathophysiology is complex as some chemokines favor tumor growth and metastasis, while others may enhance anti-tumor immunity. These diverse functions of chemokines establish them as key mediators between the tumor cells and their microenvironment and play critical role in tumor progression and metastasis. In this review, we present some of the recent advances in chemokine research with special emphasis on its role in tumor angiogenesis and metastasis.

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“…9,10 Although some chemokines are considered usually homeostatic by their implication in trafficking of specific cells under physiologic conditions, other chemokines have pro-inflammatory properties and their production is induced in response to immunologic, inflammatory, infectious signals. 11 The effective immune response against pathogens, including virus, is extensively described to be dependent of the recruitment of inflammatory cells by chemokines. [12][13][14][15] Among these chemokines, CCL3 (MIP-1 α), and its receptor CC-chemokine receptor 5 (CCR5) 10 appear to have a critical role in regulating cell recruitment to different classes of virus, including those of the genus Flavivirus, 16,17 and exhibits a variety of pro-inflammatory activities.…”

Section: Introductionmentioning

confidence: 99%

Influence of the CCR-5/MIP-1 α Axis in the Pathogenesis of Rocio Virus Encephalitis in a Mouse Model

Chávez¹,

Franca²,

Oliveira³

et al. 2013

The American Society of Tropical Medicine and Hygiene

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Abstract. Rocio virus (ROCV) caused an outbreak of human encephalitis during the 1970s in Brazil and its immunopathogenesis remains poorly understood. CC-chemokine receptor 5 (CCR5) is a chemokine receptor that binds to macrophage inflammatory protein (MIP-1 α). Both molecules are associated with inflammatory cells migration during infections. In this study, we demonstrated the importance of the CCR5 and MIP-1 α, in the outcome of viral encephalitis of ROCV-infected mice. CCR5 and MIP-1 α knockout mice survived longer than wild-type (WT) ROCV-infected animals. In addition, knockout mice had reduced inflammation in the brain. Assessment of brain viral load showed mice virus detection five days post-infection in wild-type and CCR5−/− mice, while MIP-1 α−/− mice had lower viral loads seven days postinfection. Knockout mice required a higher lethal dose than wild-type mice as well. The CCR5/MIP-1 α axis may contribute to migration of infected cells to the brain and consequently affect the pathogenesis during ROCV infection.

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The chemokine system: tuning and shaping by regulation of receptor expression and coupling in polarized responses

Cited by 68 publications

References 103 publications

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

Chemokines in tumor angiogenesis and metastasis

Influence of the CCR-5/MIP-1 α Axis in the Pathogenesis of Rocio Virus Encephalitis in a Mouse Model

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