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Journal of Virology, December 2006, p. 11998-12008, Vol. 80, No. 24
0022-538X/06/$08.00+0 doi:10.1128/JVI.01447-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Cellular and Molecular Biology, FNRS-FUSAGx, Gembloux, Belgium,1 Department of Immunology, Imperial College, London, United Kingdom,2 Zootechny Unit, FUSAGx, Gembloux, Belgium,3 U892 INRA, Jouy-en-Josas, France,4 National Veterinary Research Institute, Pulawy, Poland5
Received 10 July 2006/ Accepted 28 September 2006
Lymphocyte homeostasis is determined by a critical balance between cell proliferation and death, an equilibrium which is deregulated in bovine leukemia virus (BLV)-infected sheep. We have previously shown that an excess of proliferation occurs in lymphoid tissues and that the peripheral blood population is prone to increased cell death. To further understand the mechanisms involved, we evaluated the physiological role of the spleen in this accelerated turnover. To this end, B lymphocytes were labeled in vivo using a fluorescent marker (carboxyfluorescein diacetate succinimidyl ester), and the cell kinetic parameters (proliferation and death rates) of animals before and after splenectomy were compared. We show that the enhanced cell death observed in BLV-infected sheep is abrogated after splenectomy, revealing a key role of the spleen in B-lymphocyte dynamics.
Published ahead of print on 11 October 2006.
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