Publications
2009
Lacotte Stéphanie, Brun Susana, Muller Sylviane, Dumortier Hélène
CXCR3, inflammation, and autoimmune diseases Journal Article
In: Annals of the New York Academy of Sciences, vol. 1173, pp. 310–317, 2009, ISSN: 1749-6632.
Abstract | Links | BibTeX | Tags: Animals, arthritis, Biological, Chemokine CXCL10, Chemokine CXCL11, Chemokine CXCL9, CXCR3, Dumortier, Humans, I2CT, inflammation, Lupus Erythematosus, Models, Receptors, rheumatoid, Systemic, Team-Dumortier
@article{lacotte_cxcr3_2009,
title = {CXCR3, inflammation, and autoimmune diseases},
author = {Stéphanie Lacotte and Susana Brun and Sylviane Muller and Hélène Dumortier},
doi = {10.1111/j.1749-6632.2009.04813.x},
issn = {1749-6632},
year = {2009},
date = {2009-01-01},
journal = {Annals of the New York Academy of Sciences},
volume = {1173},
pages = {310--317},
abstract = {CXCR3 is a G protein-coupled, seven-transmembrane receptor that binds and is activated by the three IFN-gamma-inducible chemokines of the CXC family named CXCL9, CXCL10, and CXCL11. These chemokines are not constitutively expressed but are up-regulated in a proinflammatory cytokine milieu. Consequently, their major function is to selectively recruit immune cells at inflammation sites, but they also play a role in angiogenesis mechanisms. In the last few years, strong experimental and clinical evidence has been obtained supporting the idea that the CXCR3 pathway is involved in the development of autoimmune diseases, especially by creating local amplification loops of inflammation in target organs, thereby inducing worsening of clinical manifestations. This article briefly reviews what we know today about the nature and functions of CXCR3, with special emphasis on its involvement in two main rheumatic systemic autoimmune diseases, namely rheumatoid arthritis and systemic lupus erythematosus.},
keywords = {Animals, arthritis, Biological, Chemokine CXCL10, Chemokine CXCL11, Chemokine CXCL9, CXCR3, Dumortier, Humans, I2CT, inflammation, Lupus Erythematosus, Models, Receptors, rheumatoid, Systemic, Team-Dumortier},
pubstate = {published},
tppubtype = {article}
}
2005
Berthier-Vergnes Odile, Bermond Fabienne, Flacher Vincent, Massacrier Catherine, Schmitt Daniel, Péguet-Navarro Josette
TNF-alpha enhances phenotypic and functional maturation of human epidermal Langerhans cells and induces IL-12 p40 and IP-10/CXCL-10 production Journal Article
In: FEBS letters, vol. 579, no. 17, pp. 3660–3668, 2005, ISSN: 0014-5793.
Abstract | Links | BibTeX | Tags: Antigens, Apoptosis, C-Type, CD, Cell Differentiation, Cells, Chemokine CXCL10, chemokines, Cultured, CXC, Epidermal Cells, HLA-DR Antigens, Humans, Hypersensitivity, Interleukin-12, Interleukin-12 Subunit p40, Langerhans Cells, Lectins, Mannose-Binding Lectins, Phenotype, Protein Subunits, Surface, T-Lymphocytes, Team-Mueller, Tumor Necrosis Factor-alpha
@article{berthier-vergnes_tnf-alpha_2005,
title = {TNF-alpha enhances phenotypic and functional maturation of human epidermal Langerhans cells and induces IL-12 p40 and IP-10/CXCL-10 production},
author = {Odile Berthier-Vergnes and Fabienne Bermond and Vincent Flacher and Catherine Massacrier and Daniel Schmitt and Josette Péguet-Navarro},
doi = {10.1016/j.febslet.2005.04.087},
issn = {0014-5793},
year = {2005},
date = {2005-07-01},
journal = {FEBS letters},
volume = {579},
number = {17},
pages = {3660--3668},
abstract = {Dendritic cells (DC) play a central role in immunity/tolerance decision, depending on their activation/maturation state. TNF-alpha is largely produced in the skin under inflammatory conditions. However, it still remains to be defined how TNF-alpha modulates the activation status of human LC, the most specialized DC controlling skin immunity. Here, we reported that fresh immature LC, highly purified from healthy human skin and exposed for two days to TNF-alpha under serum-free conditions, expressed up-regulated level of co-stimulatory molecules (CD40, CD54, CD86), maturation markers (CD83, DC-LAMP), CCR7 lymph node homing receptor, and down-regulated Langerin level, in a dose-dependent manner. This mature phenotype is closely associated with enhanced LC allostimulatory capacity. Furthermore, TNF-alpha significantly increased the number of viable LC and decreased their spontaneous apoptosis. More importantly, TNF-alpha induced LC to produce both IFN-gamma-inducible-protein IP-10/CXCL10, a Th1-attracting chemokine and IL-12 p40. Bioactive IL-12 p70 was never detected, even after additional CD40 stimulus. The results implicate LC as an effective target through which TNF-alpha may up- or down-regulate the inflammatory skin reactions.},
keywords = {Antigens, Apoptosis, C-Type, CD, Cell Differentiation, Cells, Chemokine CXCL10, chemokines, Cultured, CXC, Epidermal Cells, HLA-DR Antigens, Humans, Hypersensitivity, Interleukin-12, Interleukin-12 Subunit p40, Langerhans Cells, Lectins, Mannose-Binding Lectins, Phenotype, Protein Subunits, Surface, T-Lymphocytes, Team-Mueller, Tumor Necrosis Factor-alpha},
pubstate = {published},
tppubtype = {article}
}