| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
* INSERM U433, IFR des Neurosciences de Lyon, Faculté de Médecine Laënnec, Lyon, France;
ENS/CNRS 5161, Laboratoires de Biologie Moléculaire de la Cellule, Lyon, France; and
Laboratoire d’Immunologie, Hôpital Neurologique, Lyon, France
2Correspondence: INSERM U433, Faculté de Médecine Laennec, 07 rue Guillaume Paradin, 69372 Lyon, France. E-mail: nataf{at}lyon.inserm.fr
Recent evidence indicates that microglial cells may not derive from blood circulating mature monocytes as they express features of myeloid progenitors. Here, we observed that a subpopulation of microglial cells expressed CD34 and B220 antigens during brain development. We thus hypothesized that microglia, or a subset of microglial cells, originate from blood circulating CD34+/B220+ myeloid progenitors, which could target the brain under developmental or neuroinflammatory conditions. Using experimental allergic encephalomyelitis (EAE) as a model of chronic neuroinflammation, we found that a discrete population of CD34+/B220+ cells expands in both blood and brain of diseased animals. In EAE mice, intravenous transfer experiments showed that macrophage-colony stimulating factor (M-CSF) -expanded CD34+ myeloid progenitors target the inflamed central nervous system (CNS) while keeping their immature phenotype. Based on these results, we then assessed whether CD34+/B220+ cells display in vitro differentiation potential toward microglia. For this purpose, CD34+/B220+ cells were sorted from M-CSF-stimulated bone marrow (BM) cultures and exposed to a glial cell conditioned medium. Under these experimental conditions, CD34+/B220+ cells were able to differentiate into microglial-like cells showing the morphological and phenotypic features of native microglia. Overall, our data suggest that under developmental or neuroinflammatory conditions, a subpopulation of microglial cells derive from CNS-invading CD34+/B220+ myeloid progenitors.—Davoust, N., Vuaillat, C., Cavillon, G., Domenget, C., Hatterer, E., Bernard, A., Dumontel, C., Jurdic, P., Malcus, C., Confavreux, C., Belin, M. F., Nataf, S. Bone marrow CD34+/B220+ progenitors target the inflamed brain and display in vitro differentiation potential toward microglia.
Key Words: glial cell • bone marrow • stem cells • cell transfer
This article has been cited by other articles:
|
|
 |
|
  V. Desestret, J.-C. Brisset, S. Moucharrafie, E. Devillard, S. Nataf, J. Honnorat, N. Nighoghossian, Y. Berthezene, and M. Wiart Early-Stage Investigations of Ultrasmall Superparamagnetic Iron Oxide-Induced Signal Change After Permanent Middle Cerebral Artery Occlusion in Mice Stroke, May 1, 2009; 40(5): 1834 - 1841. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. R. Tambuyzer, P. Ponsaerts, and E. J. Nouwen Microglia: gatekeepers of central nervous system immunology J. Leukoc. Biol., March 1, 2009; 85(3): 352 - 370. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Vuaillat, G. Androdias, N. Davoust, and S. Nataf About multiple sclerosis, natalizumab, and CD34+ hematopoietic progenitors Blood, July 1, 2008; 112(1): 208 - 209. [Full Text] [PDF]
|
|
|
|
 |
|
 J. Palazuelos, N. Davoust, B. Julien, E. Hatterer, T. Aguado, R. Mechoulam, C. Benito, J. Romero, A. Silva, M. Guzman, et al. The CB2 Cannabinoid Receptor Controls Myeloid Progenitor Trafficking: INVOLVEMENT IN THE PATHOGENESIS OF AN ANIMAL MODEL OF MULTIPLE SCLEROSIS J. Biol. Chem., May 9, 2008; 283(19): 13320 - 13329. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
