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Kumar A.,Institute Of Gene Tique Et Of Biologie Mole Culaire Et Cellulaire | Kumar A.,French National Center for Scientific Research | Kumar A.,Institute National Of La Sante Et Of La Recherche Me Dicale | Kumar A.,University of Strasbourg | And 14 more authors.
Journal of Cell Science

Cell migration is an essential and highly regulated process. During development, glia cells and neurons migrate over long distances - in most cases collectively - to reach their final destination and buildthe sophisticated architecture of the nervous system, the most complex tissue of the body. Collective migration is highlystereotyped and efficient, defects in the process leading to severe human diseases that include mental retardation. This dynamic process entails extensive cell communication and coordination, hence, the real challenge is to analyze it in the entire organism and at cellular resolution. We here investigate the impact of the Ncadherin adhesion molecule on collective glial migration, by using the Drosophila developing wing and cell-type specific manipulation of gene expression. We show that N-cadherin timely accumulates in glial cells and that its levels affect migration efficiency. N-cadherin works as a molecular brake in a dosage-dependent manner, by negatively controlling actin nucleation and cytoskeleton remodeling through a/b catenins. This is the first in vivo evidence for N-cadherin negatively and cell autonomously controlling collective migration. © 2015. Published by The Company of Biologists Ltd. Source

Guillerey C.,Institute Pasteur Paris | Guillerey C.,French Institute of Health and Medical Research | Guillerey C.,University Paris Diderot | Mouries J.,Institute Pasteur Paris | And 11 more authors.

The physiologic role played by plasmacytoid dendritic cells (pDCs) in the induction of innate responses and inflammation in response to pathogen signaling is not well understood. Here, we describe a new mouse model lacking pDCs and establish that pDCs are essential for the in vivo induction of NK-cell activity in response to Toll-like receptor 9 (TLR9) triggering. Furthermore, we provide the first evidence that pDCs are critical for the systemic production of a wide variety of chemokines in response to TLR9 activation. Consequently, we observed a profound alteration in monocyte, macrophage, neutrophil, and NK-cell recruitment at the site of inflammation in the absence of pDCs in response to CpG-Dotap and stimulation by microbial pathogens, such as Leishmania major, Escherichia coli, and Mycobacterium bovis. This study, which is based on the development of a constitutively pDC-deficient mouse model, highlights the pivotal role played by pDCs in the induction of innate immune responses and inflammation after TLR9 triggering. © 2012 by The American Society of Hematology. Source

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