Navet Benjamin, Vargas-Franco Jorge William, Gama Andrea, Amiaud Jérome, Choi Yongwon, Yagita Hideo, Mueller Christopher G, Rédini Françoise, Heymann Dominique, Castaneda Beatriz, Lézot Frédéric
Maternal RANKL Reduces the Osteopetrotic Phenotype of Null Mutant Mouse Pups Journal Article
In: Journal of Clinical Medicine, vol. 7, no. 11, 2018, ISSN: 2077-0383.
Abstract | Links | BibTeX | Tags: bone, mandible, Morphogenesis, OSTEOCLAST, RANKL, skeletal growth, Team-Mueller, Tooth
@article{navet_maternal_2018,
title = {Maternal RANKL Reduces the Osteopetrotic Phenotype of Null Mutant Mouse Pups},
author = {Benjamin Navet and Jorge William Vargas-Franco and Andrea Gama and Jérome Amiaud and Yongwon Choi and Hideo Yagita and Christopher G Mueller and Françoise Rédini and Dominique Heymann and Beatriz Castaneda and Frédéric Lézot},
doi = {10.3390/jcm7110426},
issn = {2077-0383},
year = {2018},
date = {2018-11-01},
journal = {Journal of Clinical Medicine},
volume = {7},
number = {11},
abstract = {RANKL signalization is implicated in the morphogenesis of various organs, including the skeleton. Mice invalidated for Rankl present an osteopetrotic phenotype that was less severe than anticipated, depending on RANKL's implication in morphogenesis. The hypothesis of an attenuated phenotype, as a result of compensation during gestation by RANKL of maternal origin, was thus brought into question. In order to answer this question, Rankl null mutant pups from null mutant parents were generated, and the phenotype analyzed. The results validated the presence of a more severe osteopetrotic phenotype in the second-generation null mutant with perinatal lethality. The experiments also confirmed that RANKL signalization plays a part in the morphogenesis of skeletal elements through its involvement in cell-to-cell communication, such as in control of osteoclast differentiation. To conclude, we have demonstrated that the phenotype associated with Rankl invalidation is attenuated through compensation by RANKL of maternal origin.},
keywords = {bone, mandible, Morphogenesis, OSTEOCLAST, RANKL, skeletal growth, Team-Mueller, Tooth},
pubstate = {published},
tppubtype = {article}
}
Mueller C G, Nayar S, Campos J, Barone F
Molecular and Cellular Requirements for the Assembly of Tertiary Lymphoid Structures Journal Article
In: Advances in Experimental Medicine and Biology, vol. 1060, pp. 55–72, 2018, ISSN: 0065-2598.
Abstract | Links | BibTeX | Tags: 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}
}
Lézot Frédéric, Chesneau Julie, Navet Benjamin, Gobin Bérengère, Amiaud Jérome, Choi YongWon, Yagita Hideo, Castaneda Beatriz, Berdal Ariane, Mueller Christopher G, Rédini Françoise, Heymann Dominique
In: Bone, vol. 73, pp. 51–59, 2015, ISSN: 1873-2763.
Abstract | Links | BibTeX | Tags: Animals, Antibodies, Bone Density Conservation Agents, Bone Development, Bone resorption, Diphosphonates, Female, Imidazoles, Inbred C57BL, Mice, Newborn, Pregnancy, RANK ligand, RANKL, Side effect, Skeleton growth, Team-Mueller, Tooth Eruption, Zoledronic acid
@article{lezot_skeletal_2015,
title = {Skeletal consequences of RANKL-blocking antibody (IK22-5) injections during growth: mouse strain disparities and synergic effect with zoledronic acid},
author = {Frédéric Lézot and Julie Chesneau and Benjamin Navet and Bérengère Gobin and Jérome Amiaud and YongWon Choi and Hideo Yagita and Beatriz Castaneda and Ariane Berdal and Christopher G Mueller and Françoise Rédini and Dominique Heymann},
doi = {10.1016/j.bone.2014.12.011},
issn = {1873-2763},
year = {2015},
date = {2015-01-01},
journal = {Bone},
volume = {73},
pages = {51--59},
abstract = {High doses of bone resorption inhibitors are currently under evaluation in pediatric oncology. Previous works have evidenced transient arrest in long bone and skull bone growth and tooth eruption blockage when mice were treated with zoledronic acid (ZOL). The question of potential similar effects with a RANKL-blocking antibody (IK22.5) was raised. Sensitivity disparities in these inhibitors between mouse strains and synergic effects of zoledronic acid and a RANKL-blocking antibody were subsidiary questions. In order to answer these questions, newborn C57BL/6J and CD1 mice were injected every two or three days (4 injections in total so 7 or 10 days of treatment length) with high doses of a RANKL-blocking antibody. The consequences on the tibia, craniofacial bones and teeth were analyzed by μCT and histology at the end of the treatment and one, two and three months later. The results obtained showed that RANKL-blocking antibody injections induced a transient arrest of tibia and skull bone growth and an irreversible blockage of tooth eruption in C57BL/6J mice. In CD1 mice, tooth eruption defects were also present but only at much higher doses. Similar mouse strain differences were obtained with zoledronic acid. Finally, a synergic effect of the two inhibitors was evidenced. In conclusion as previously observed for bisphosphonates (ZOL), a RANKL-blocking antibody induced a transient arrest in long bone and skull bone growth and a blockage of tooth eruption with however disparities between mouse strains with regard to this last effect. A synergic effect of both bone resorption inhibitors was also demonstrated.},
keywords = {Animals, Antibodies, Bone Density Conservation Agents, Bone Development, Bone resorption, Diphosphonates, Female, Imidazoles, Inbred C57BL, Mice, Newborn, Pregnancy, RANK ligand, RANKL, Side effect, Skeleton growth, Team-Mueller, Tooth Eruption, Zoledronic acid},
pubstate = {published},
tppubtype = {article}
}