Mueller C G, Nayar S, Campos J, Barone F
Molecular and Cellular Requirements for the Assembly of Tertiary Lymphoid Structures Article de journal
Dans: Advances in Experimental Medicine and Biology, vol. 1060, p. 55–72, 2018, ISSN: 0065-2598.
Résumé | Liens | BibTeX | Étiquettes: Animals, CCL21, CXCL13, Endothelial and stromal cells, Humans, Lymphotoxin, Molecular Targeted Therapy, RANKL, Sjögren’s syndrome, Team-Mueller, Tertiary lymphoid structures, TNF
@article{mueller_molecular_2018,
title = {Molecular and Cellular Requirements for the Assembly of Tertiary Lymphoid Structures},
author = {C G Mueller and S Nayar and J Campos and F Barone},
doi = {10.1007/978-3-319-78127-3_4},
issn = {0065-2598},
year = {2018},
date = {2018-01-01},
journal = {Advances in Experimental Medicine and Biology},
volume = {1060},
pages = {55--72},
abstract = {At sites of chronic inflammation, recruited immune cells form structures that resemble secondary lymphoid organs (SLOs). Those are characterized by segregated areas of prevalent T- or B-cell aggregation, differentiation of high endothelial venules (HEVs) and local activation of resident stromal cells. B-cell proliferation and affinity maturation towards locally displayed autoantigens have been demonstrated at those sites, known as tertiary lymphoid structures (TLSs). TLS formation has been associated with local disease persistence and progression as well as increased systemic manifestations. While bearing a similar histological structure to SLO, the signals that regulate TLS and SLO formation can diverge, and a series of pro-inflammatory cytokines has been ascribed as responsible for TLS formation at different anatomical sites. Here we review the structural elements as well as the signals responsible for TLS aggregation, aiming to provide an overview to this complex immunological phenomenon.},
keywords = {Animals, CCL21, CXCL13, Endothelial and stromal cells, Humans, Lymphotoxin, Molecular Targeted Therapy, RANKL, Sjögren’s syndrome, Team-Mueller, Tertiary lymphoid structures, TNF},
pubstate = {published},
tppubtype = {article}
}
Mueller Christopher George, Nayar Saba, Gardner David, Barone Francesca
Cellular and Vascular Components of Tertiary Lymphoid Structures Article de journal
Dans: Methods in Molecular Biology (Clifton, N.J.), vol. 1845, p. 17–30, 2018, ISSN: 1940-6029.
Résumé | Liens | BibTeX | Étiquettes: Animals, Biomarkers, CCL21, Cell Survival, Cellular Microenvironment, CXCL13, Cytokines, Humans, Immunity, inflammation, Innate, LYMPHATIC VESSEL, Lymphocyte, Lymphocyte Subsets, Lymphotoxin, Multigene Family, Neovascularization, Pathologic, Receptors, Signal Transduction, Sjögren’s syndrome, Stromal cell, Team-Mueller, Tertiary lymphoid organ, Tertiary lymphoid structures, TNF-α, Tumor Necrosis Factor
@article{mueller_cellular_2018,
title = {Cellular and Vascular Components of Tertiary Lymphoid Structures},
author = {Christopher George Mueller and Saba Nayar and David Gardner and Francesca Barone},
doi = {10.1007/978-1-4939-8709-2_2},
issn = {1940-6029},
year = {2018},
date = {2018-01-01},
journal = {Methods in Molecular Biology (Clifton, N.J.)},
volume = {1845},
pages = {17--30},
abstract = {Inflammatory immune cells recruited at the site of chronic inflammation form structures that resemble secondary lymphoid organs (SLO). These are characterized by segregated areas of prevalent T- or B-cell aggregation, differentiation of high endothelial venules, and local activation of resident stromal cells, including lymphatic endothelial cells. B-cell proliferation and affinity maturation toward locally displayed autoantigens have been demonstrated at these sites, known as tertiary lymphoid structures (TLS). TLS formation during chronic inflammation has been associated with local disease persistence and progression, as well as increased systemic manifestations. While bearing a similar histological structure to SLO, the signals that regulate TLS and SLO formation can diverge and a series of pro-inflammatory cytokines have been ascribed as responsible for TLS formation at different anatomical sites. Moreover, for a long time the structural compartment that regulates TLS homeostasis, including survival and recirculation of leucocytes has been neglected. In this chapter, we summarize the novel data available on TLS formation, structural organization, and the functional and anatomical links connecting TLS and SLOs.},
keywords = {Animals, Biomarkers, CCL21, Cell Survival, Cellular Microenvironment, CXCL13, Cytokines, Humans, Immunity, inflammation, Innate, LYMPHATIC VESSEL, Lymphocyte, Lymphocyte Subsets, Lymphotoxin, Multigene Family, Neovascularization, Pathologic, Receptors, Signal Transduction, Sjögren’s syndrome, Stromal cell, Team-Mueller, Tertiary lymphoid organ, Tertiary lymphoid structures, TNF-α, Tumor Necrosis Factor},
pubstate = {published},
tppubtype = {article}
}
Cordeiro Olga G, Chypre Mélanie, Brouard Nathalie, Rauber Simon, Alloush Farouk, Romera-Hernandez Monica, Bénézech Cécile, Li Zhi, Eckly Anita, Coles Mark C, Rot Antal, Yagita Hideo, Léon Catherine, Ludewig Burkhard, Cupedo Tom, Lanza François, Mueller Christopher G
Integrin-Alpha IIb Identifies Murine Lymph Node Lymphatic Endothelial Cells Responsive to RANKL Article de journal
Dans: PloS One, vol. 11, no. 3, p. e0151848, 2016, ISSN: 1932-6203.
Résumé | Liens | BibTeX | Étiquettes: Activation, Animals, Cells, Cultured, Endothelial Cells, ENDOTHELIAL-CELLS, Expression, Fibronectins, Immunization, Immunology, immunopathology, Inbred C57BL, infection, ligand, LYMPH, LYMPH NODE, Lymph Nodes, lymphoid organs, Lymphotoxin, Lymphotoxin-beta, Mice, murine, NF-kappaB, Platelet Membrane Glycoprotein IIb, PLATELETS, PROGENITORS, rank, RANK ligand, Receptor, Secondary, Signal Transduction, signaling, SINUS, Team-Mueller
@article{cordeiro_integrin-alpha_2016,
title = {Integrin-Alpha IIb Identifies Murine Lymph Node Lymphatic Endothelial Cells Responsive to RANKL},
author = {Olga G Cordeiro and Mélanie Chypre and Nathalie Brouard and Simon Rauber and Farouk Alloush and Monica Romera-Hernandez and Cécile Bénézech and Zhi Li and Anita Eckly and Mark C Coles and Antal Rot and Hideo Yagita and Catherine Léon and Burkhard Ludewig and Tom Cupedo and François Lanza and Christopher G Mueller},
doi = {10.1371/journal.pone.0151848},
issn = {1932-6203},
year = {2016},
date = {2016-01-01},
journal = {PloS One},
volume = {11},
number = {3},
pages = {e0151848},
abstract = {Microenvironment and activation signals likely imprint heterogeneity in the lymphatic endothelial cell (LEC) population. Particularly LECs of secondary lymphoid organs are exposed to different cell types and immune stimuli. However, our understanding of the nature of LEC activation signals and their cell source within the secondary lymphoid organ in the steady state remains incomplete. Here we show that integrin alpha 2b (ITGA2b), known to be carried by platelets, megakaryocytes and hematopoietic progenitors, is expressed by a lymph node subset of LECs, residing in medullary, cortical and subcapsular sinuses. In the subcapsular sinus, the floor but not the ceiling layer expresses the integrin, being excluded from ACKR4+ LECs but overlapping with MAdCAM-1 expression. ITGA2b expression increases in response to immunization, raising the possibility that heterogeneous ITGA2b levels reflect variation in exposure to activation signals. We show that alterations of the level of receptor activator of NF-κB ligand (RANKL), by overexpression, neutralization or deletion from stromal marginal reticular cells, affected the proportion of ITGA2b+ LECs. Lymph node LECs but not peripheral LECs express RANK. In addition, we found that lymphotoxin-β receptor signaling likewise regulated the proportion of ITGA2b+ LECs. These findings demonstrate that stromal reticular cells activate LECs via RANKL and support the action of hematopoietic cell-derived lymphotoxin.},
keywords = {Activation, Animals, Cells, Cultured, Endothelial Cells, ENDOTHELIAL-CELLS, Expression, Fibronectins, Immunization, Immunology, immunopathology, Inbred C57BL, infection, ligand, LYMPH, LYMPH NODE, Lymph Nodes, lymphoid organs, Lymphotoxin, Lymphotoxin-beta, Mice, murine, NF-kappaB, Platelet Membrane Glycoprotein IIb, PLATELETS, PROGENITORS, rank, RANK ligand, Receptor, Secondary, Signal Transduction, signaling, SINUS, Team-Mueller},
pubstate = {published},
tppubtype = {article}
}