Reference : Follicular dendritic cells control engulfment of apoptotic bodies by secreting Mfge8.
Scientific journals : Article
Life sciences : Anatomy (cytology, histology, embryology...) & physiology
http://hdl.handle.net/2268/23320
Follicular dendritic cells control engulfment of apoptotic bodies by secreting Mfge8.
English
Kranich, Jan [> > > >]
Krautler, Nike Julia [> > > >]
Heinen, Ernst mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Histologie humaine >]
Polymenidou, Magdalini [> > > >]
Bridel, Claire [> > > >]
Schildknecht, Anita [> > > >]
Huber, Christoph [> > > >]
Kosco-Vilbois, Marie H [> > > >]
Zinkernagel, Rolf [> > > >]
Miele, Gino [> > > >]
Aguzzi, Adriano [> > > >]
2008
Journal of Experimental Medicine
Rockefeller University Press
205
6
1293-302
Yes (verified by ORBi)
International
0022-1007
1540-9538
New York
NY
[en] Animals ; Antibodies/immunology ; Antigens, CD45/immunology ; Antigens, Surface/genetics ; Apoptosis/physiology ; B-Lymphocytes/cytology/immunology/physiology ; Bone Marrow Transplantation ; Crosses, Genetic ; DNA Primers ; Dendritic Cells/immunology ; Dendritic Cells, Follicular/cytology/physiology ; In Situ Hybridization ; In Situ Nick-End Labeling ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred Strains ; Mice, Knockout ; Milk Proteins/genetics/secretion ; RNA/genetics ; Receptors, Complement 3d/immunology
[en] The secreted phosphatidylserine-binding protein milk fat globule epidermal growth factor 8 (Mfge8) mediates engulfment of apoptotic germinal center B cells by tingible-body macrophages (TBMphis). Impairment of this process can contribute to autoimmunity. We show that Mfge8 is identical to the mouse follicular dendritic cell (FDC) marker FDC-M1. In bone-marrow chimeras between wild-type and Mfge8(-/-) mice, all splenic Mfge8 was derived from FDCs rather than TBMphis. However, Mfge8(-/-) TBMphis acquired and displayed Mfge8 only when embedded in Mfge8(+/+) stroma, or when situated in lymph nodes draining exogenous recombinant Mfge8. These findings indicate a licensing role for FDCs in TBMphi-mediated removal of excess B cells. Lymphotoxin-deficient mice lacked FDCs and splenic Mfge8, and suffer from autoimmunity similar to Mfge8(-/-) mice. Hence, FDCs facilitate TBMphi-mediated corpse removal, and their malfunction may be involved in autoimmunity.
http://hdl.handle.net/2268/23320
10.1084/jem.20071019

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