Alteration of B-cell subsets enhances neuroinvasion in mouse scrapie infection.
Acquired forms of prion diseases or transmissible spongiform encephalopathies are believed to occur following peripheral exposure. Prions initially accumulate in the lymphoid system before spreading to the nervous system, but the underlying mechanisms for prion transfer between the two systems are still elusive. Here we show that ablation of the B-cell-specific transmembrane protein CD19, a coreceptor of the complement system, results in an acceleration of prion neuroinvasion. This appears to be due to an alteration of the follicular dendritic cell (FDC) network within the lymphoid tissue, thereby reducing the distance between FDCs and adjacent nerve fibers that mediate prion neuroinvasion.
von Poser-Klein
Christine
C
Institute of Virology and Immunobiology, University of Würzburg, Versbacherstr. 7, D-97078 Würzburg, Germany.
Flechsig
Eckhard
E
Hoffmann
Tanja
T
Schwarz
Petra
P
Harms
Harry
H
Bujdoso
Raymond
R
Aguzzi
Adriano
A
Klein
Michael A
MA
D000818:Animals; D018941:Antigens, CD19 / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D003713:Dendritic Cells / Q000276:immunology; D008221:Lymphoid Tissue / Q000166:cytology; D051379:Mice; D018345:Mice, Knockout; D009422:Nervous System Diseases / Q000276:immunology*; D018620:PrPSc Proteins / Q000032:analysis / Q000302:isolation & purification; D012608:Scrapie / Q000276:immunology*; D013154:Spleen / Q000737:chemistry; D016019:Survival Analysis
D018941:Antigens, CD19; D018620:PrPSc Proteins