Subscribe to the World's Most Popular Newsletter (it's free!)
Borrelia burgdorferi (Bb) is the tick-borne etiologic agent of
Lyme borreliosis, which has many aspects of autoimmune diseases. Bb is unable to recycle synthesized membrane lipids and lipoproteins. Consequently, a large amount of liposome-like vesicle (Bb-blebs) is shed from the outer bacterial membrane. The influence of Bb-blebs on the cellular immune response is not yet known. As a Bb-blebs model, we established standardized Bb-liposomes, produced from freshly extracted lipids and lipoproteins of live Bb. Bb-liposomes were incorporated via nonendocytotic mechanisms by different human cell types, namely dendritic cells (DC), lymphocytes, and fibroblasts, as visualized by immunofluorescence and transmission electron microscopy. Bb-liposomes were localized in the cytosol and in the nucleus of the cells. With this in mind, we generated in vitro Bb-specific T-cells from nonadherant peripheral blood mononuclear cells by use of Bb-liposomes loaded autologous DC. More than 95% of those T-cells were CD8(+) and they killed autologous Bb-liposome-loaded T-cell blasts. These results suggest that Bb-blebs may be responsible for the autoimmune-like appearance of
Copyright 2000 Academic Press.