UNIGE document Scientific Article
previous document  unige:11599  next document
add to browser collection

Suppression of experimental lupus nephritis by aberrant expression of the soluble E-selectin gene

Takahashi, Satoru
Araki, Kimi
Araki, Masatake
Ito, M. R.
Nakatani, Kimihiko
Fujii, Hiroshi
show hidden authors show all authors [1 - 9]
Published in Pathology International. 2002, vol. 52, no. 3, p. 175-180
Abstract Circulating leukocytes, particularly neutrophils and monocytes, are important effector cells in the induction of many forms of glomerulonephritis. Adhesion molecules, especially selectins, are also thought to be critical for the development of this disease. We examined the possible suppressive effect of soluble E-selectin on the development of experimental lupus nephritis induced by the injection of a hybridoma clone (2B11.3) derived from an MRL/MpJ-lpr/lpr lupus mouse. This clone produces IgG3 antibodies that induce severe proliferative glomerulonephritis resembling lupus nephritis when injected into normal mice. Transgenic mice with a soluble E-selectin gene were injected intraperitoneally with the hybridoma cells and histopathologically examined on day 15. As a result, the development of glomerulonephritis was significantly suppressed. This suppression was characterized by fewer inflammatory cell infiltrates, compared with non-transgenic litter mates, despite the fact that there were no remarkable differences in immunoglobulin deposits or expression of E-selectin between the two groups. These findings suggest that by controlling inflammatory cell infiltration, soluble E-selectin plays a preventative role in the development of a particular type of lupus nephritis.
Keywords AnimalsAntibodies, Monoclonal/pharmacologyDisease Models, AnimalE-Selectin/ genetics/immunologyHybridomas/immunology/pathology/transplantationImmunoglobulin G/blood/geneticsLupus Nephritis/immunology/pathology/ prevention & controlMiceMice, Inbred BALB CMice, Inbred DBAMice, Transgenic
Stable URL http://archive-ouverte.unige.ch/unige:11599
Full text
PMID: 11972860
95 hits and 0 download since 2010-08-27
Export document
Format :
Citation style :