Publications
2008
Barbaroux J B, Beleut M, Brisken C, Mueller C G, Groves R W
Epidermal receptor activator of NF-kappaB ligand controls Langerhans cells numbers and proliferation Article de journal
Dans: Journal of Immunology, vol. 181, no. 1550-6606 (Electronic), p. 1103–1108, 2008.
Résumé | BibTeX | Étiquettes: APC, Apoptosis, BLOOD, Cell Count, Cell Proliferation, Cell Survival, Culture, cytology, Dendritic Cells, DERMATOLOGY, Differentiation, Epidermis, Expression, Homeostasis, Human, Humans, Immunology, IN VITRO, In vivo, KERATINOCYTES, Langerhans Cells, ligand, metabolism, Mice, NF-kappa B, NF-kappaB, OSTEOCLAST, Osteoclasts, Proliferation, Protein, rank, RANK ligand, Receptor, Receptor Activator of Nuclear Factor-kappa B, Regulation, Signal Transduction, Skin, survival, Team-Mueller, viability
@article{barbaroux_epidermal_2008,
title = {Epidermal receptor activator of NF-kappaB ligand controls Langerhans cells numbers and proliferation},
author = {J B Barbaroux and M Beleut and C Brisken and C G Mueller and R W Groves},
year = {2008},
date = {2008-01-01},
journal = {Journal of Immunology},
volume = {181},
number = {1550-6606 (Electronic)},
pages = {1103--1108},
abstract = {Langerhans cells (LC) are the dendritic APC population of the epidermis, where they reside for long periods and are self-replicating. The molecular signals underlying these characteristics are unknown. The TNF superfamily member receptor activator of NF-kappaB ligand (RANKL, TNFSF11) has been shown to sustain viability of blood dendritic cells in addition to its role in promoting proliferation and differentiation of several cell types, notably osteoclasts. In this study, we have studied expression of the RANKL system in skin and have defined a key role for this molecule in LC homeostasis. In vitro and in vivo, human KC expressed RANKL and epidermal LC expressed cell surface RANK. In vitro, RANKL sustained CD34(+) progenitor-derived LC viability following 72-h cultures in cytokine-free medium (79.5 +/- 1% vs 55.2 +/- 5.7% live cells, respectively; n = 4; p textless 0.05). In vivo, RANKL-deficient mice displayed a marked reduction in epidermal LC density (507.1 +/- 77.2 vs 873.6 +/- 41.6 LC per mm(2); n = 9; p textless 0.05) and their proliferation was impaired without a detectable effect on apoptosis. These data indicate a key role for the RANKL system in the regulation of LC survival within the skin and suggest a regulatory role for KC in the maintenance of epidermal LC homeostasis},
keywords = {APC, Apoptosis, BLOOD, Cell Count, Cell Proliferation, Cell Survival, Culture, cytology, Dendritic Cells, DERMATOLOGY, Differentiation, Epidermis, Expression, Homeostasis, Human, Humans, Immunology, IN VITRO, In vivo, KERATINOCYTES, Langerhans Cells, ligand, metabolism, Mice, NF-kappa B, NF-kappaB, OSTEOCLAST, Osteoclasts, Proliferation, Protein, rank, RANK ligand, Receptor, Receptor Activator of Nuclear Factor-kappa B, Regulation, Signal Transduction, Skin, survival, Team-Mueller, viability},
pubstate = {published},
tppubtype = {article}
}
2007
Mueller C G, Boix C, Kwan W H, Daussy C, Fournier E, Fridman W H, Molina T J
Critical role of monocytes to support normal B cell and diffuse large B cell lymphoma survival and proliferation Article de journal
Dans: Journal of Leukocyte Biology, vol. 82, no. 0741-5400 (Print), p. 567–575, 2007.
Résumé | BibTeX | Étiquettes: Activation, Antigen, Antigens, B CELL ACTIVATION, B CELLS, B-Cell, B-Cell Activation Factor Receptor, B-Lymphocytes, Biological, BLOOD, CC, CD14, CD40, Cell Division, Cell Proliferation, Cell Survival, Chemokine CCL5, chemokines, Coculture, cytology, Dendritic Cells, Differentiation, Diffuse, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Human, Humans, IL-2, Immunoenzyme Techniques, Interleukin-2, Large B-Cell, Lymph Nodes, LYMPHOMA, metabolism, monocyte, Monocytes, Myeloid Cells, pathology, Proliferation, Protein, Receptor, Reverse Transcriptase Polymerase Chain Reaction, survival, Team-Mueller, tumor, Tumor Markers
@article{mueller_critical_2007,
title = {Critical role of monocytes to support normal B cell and diffuse large B cell lymphoma survival and proliferation},
author = {C G Mueller and C Boix and W H Kwan and C Daussy and E Fournier and W H Fridman and T J Molina},
year = {2007},
date = {2007-01-01},
journal = {Journal of Leukocyte Biology},
volume = {82},
number = {0741-5400 (Print)},
pages = {567--575},
abstract = {Large B cell lymphomas can comprise numerous CD14+ cells in the tumor stroma, which raises the question of whether monocytes can support B cell survival and proliferation. We show that the coculture of monocytes with B cells from peripheral blood or from diffuse large B cell lymphoma enabled prolonged B cell survival. Under these conditions, diffuse large lymphoma B cells proliferated, and addition of B cell-activating factor of the TNF family (BAFF) and IL-2 enhanced cell division. Monocytes and dendritic cells (DC) had similar antiapoptotic activity on healthy B cells but displayed differences with respect to B cell proliferation. Monocytes and cord blood-derived CD14+ cells promoted B cell proliferation in the presence of an anti-CD40 stimulus, whereas DC supported B cell proliferation when activated through the BCR. DC and CD14+ cells were able to induce plasmocyte differentiation. When B cells were activated via the BCR or CD40, they released the leukocyte attractant CCL5, and this chemokine is one of the main chemokines expressed in diffuse large B cell lymphoma. The data support the notion that large B cell lymphoma recruit monocytes via CCL5 to support B cell survival and proliferation},
keywords = {Activation, Antigen, Antigens, B CELL ACTIVATION, B CELLS, B-Cell, B-Cell Activation Factor Receptor, B-Lymphocytes, Biological, BLOOD, CC, CD14, CD40, Cell Division, Cell Proliferation, Cell Survival, Chemokine CCL5, chemokines, Coculture, cytology, Dendritic Cells, Differentiation, Diffuse, Enzyme-Linked Immunosorbent Assay, Flow Cytometry, Human, Humans, IL-2, Immunoenzyme Techniques, Interleukin-2, Large B-Cell, Lymph Nodes, LYMPHOMA, metabolism, monocyte, Monocytes, Myeloid Cells, pathology, Proliferation, Protein, Receptor, Reverse Transcriptase Polymerase Chain Reaction, survival, Team-Mueller, tumor, Tumor Markers},
pubstate = {published},
tppubtype = {article}
}
2002
Cremer I, Dieu-Nosjean M C, Mar�chal S, Dezutter-Dambuyant C, Goddard S, Adams D, Winter N, Menetrier-Caux C, Saut�s-Fridman C, Fridman W H, Mueller C G F
Long-lived immature dendritic cells mediated by TRANCE-RANK interaction Article de journal
Dans: Blood, vol. 100, no. 10, p. 3646–3655, 2002.
Résumé | BibTeX | Étiquettes: Activation, Antigen, CD40, CD40 Ligand, CHEMOTAXIS, Cytokines, Dendritic Cells, Epidermis, Expression, Homeostasis, Human, IMMATURE, l, ligand, lipopolysaccharide, Longevity, LPS, LYMPH, LYMPH NODE, Lymph Nodes, M-CSF, Macrophage, Macrophages, Maturation, naive, Necrosis, NF-kappaB, PROGENITOR CELLS, rank, Receptor, survival, T CELL ACTIVATION, T CELLS, Team-Mueller, TRANCE, tumor, viability
@article{cremer_long-lived_2002,
title = {Long-lived immature dendritic cells mediated by TRANCE-RANK interaction},
author = {I Cremer and M C Dieu-Nosjean and S Mar�chal and C Dezutter-Dambuyant and S Goddard and D Adams and N Winter and C Menetrier-Caux and C Saut�s-Fridman and W H Fridman and C G F Mueller},
year = {2002},
date = {2002-01-01},
journal = {Blood},
volume = {100},
number = {10},
pages = {3646--3655},
abstract = {Immature dendritic cells (DCs) reside in Interstitial tissues (Int-DC) or in the epidermis, where they capture antigen and, thereafter, mature and migrate to draining lymph nodes (LNs), where they present processed antigen to T cells. We have Identified Int-DCs that express both TRANCE (tumor necrosis factor-related activation-induced cytokine) and RANK (receptor activator of NF-kappaB) and have generated these cells from CD34(+) human progenitor cells using macrophage colony-stimulating factor (M-CSF). These CD34(+)-derived Int-DCs, which are related to macrophages, are long-lived, but addition of soluble RANK leads to significant reduction of cell viability and BcI-2 expression. This suggests that constitutive TRANCE-RANK interaction is responsible for CD34(+)-derived Int-DC longevity. Conversely, CD1a(+) DCs express only RANK and are short-lived. However, they can be rescued from cell death either by recombinant soluble TRANCE or by CD34(+)-derived Int-DCs. CD34(+)-derived Int-DCs mature in response to lipopolysaccharide (LPS) plus CD40 ligand (L) and become capable of CCL21/CCL19-mediated chemotaxis and naive T-cell activation. Upon maturation, they lose TRANCE, making them, like CD1a(+) DCs, dependent on exogenous TRANCE for survival. These findings provide evidence that TRANCE and RANK play important roles in the homeostasis of DCs. (C) 2002 by The American Society of Hematology},
keywords = {Activation, Antigen, CD40, CD40 Ligand, CHEMOTAXIS, Cytokines, Dendritic Cells, Epidermis, Expression, Homeostasis, Human, IMMATURE, l, ligand, lipopolysaccharide, Longevity, LPS, LYMPH, LYMPH NODE, Lymph Nodes, M-CSF, Macrophage, Macrophages, Maturation, naive, Necrosis, NF-kappaB, PROGENITOR CELLS, rank, Receptor, survival, T CELL ACTIVATION, T CELLS, Team-Mueller, TRANCE, tumor, viability},
pubstate = {published},
tppubtype = {article}
}