Imaging

@article{mueller_skin_2019,

title = {Of skin and bone: did Langerhans cells and osteoclasts evolve from a common ancestor?},

author = {Christopher G Mueller and Benjamin Voisin},

doi = {10.1111/joa.12543},

issn = {1469-7580},

year  = {2019},

date = {2019-08-01},

journal = {Journal of Anatomy},

volume = {235},

number = {2},

pages = {412--417},

abstract = {Skin Langerhans cells are antigen-presenting cells of the interfollicular epidermis and the upper part of the hair follicle, whereas osteoclasts are specialized bone-resorbing macrophages. Although at first view these two cell types appear to have little in common, a closer analysis reveals shared features, and when taking into account their surrounding environment, a hypothesis can be developed that Langerhans cells and osteoclasts have evolved from a common ancestral cell type. In this mini-review, we have compared the ontogenetic features of Langerhans cells and osteoclasts from a genetic and a functional point of view, an issue that so far has been overlooked. The gene programs that control cell differentiation, and the body parts where they reside, present surprising similarities. Whereas the function of osteoclasts in bone degradation has been established since the first vertebrates, Langerhans cells may have undergone a stepwise adaptation from aquatic to terrestrial life. Their cell function co-evolved with the imperatives of the skin to protect against physical impact, heat, water loss and pathogens, which implied the capacity of Langerhans cells to associate with skin appendages and to develop immunostimulatory functions. For the highly versatile and efficient immune system of modern vertebrates, Langerhans cells may be a memory of the past.},

keywords = {Animals, Biological Evolution, Dendritic cell, Evolution, hair follicle, Humans, Langerhans cell, Langerhans Cells, Macrophage, OSTEOCLAST, Osteoclasts, Team-Mueller},

pubstate = {published},

tppubtype = {article}

}

@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}

}

@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}

}