Zobrazeno 1 - 10
of 19
pro vyhledávání: '"V R, Kelley"'
Publikováno v:
The Journal of Immunology. 157:427-432
The lpr mutation on the MRL background accelerates autoimmune nephritis in which macrophage (M phi) accumulation is prominent. Renal disease is absent in other strains with lpr. TNF-alpha and CSF-1 are increased in the kidney of MRL-lpr mice with los
Publikováno v:
The Journal of Immunology. 157:433-440
Mice with the MRL background have a genetic propensity for autoimmune lupus nephritis. The lpr mutation on the MRL, but not the C3H background, induces rapid and fatal renal injury in which macrophages (M phi) are prominent. We previously established
Publikováno v:
The Journal of Immunology. 156:4961-4968
The lpr mutation, a disruption of the fas gene, induces spontaneous autoimmunity characterized by high titers of autoantibodies, lymphadenopathy, autoreactive T cells, and early mortality. The mechanism of autoimmunity, however, remains unknown. The
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 163(12)
IL-12 is secreted by kidney tubular epithelial cells in autoimmune MRL-Fas(lpr) mice before renal injury and increases with advancing disease. Because IL-12 is a potent inducer of IFN-gamma, the purpose of this study was to determine whether local pr
Autor:
M H, Foster, V R, Kelley
Publikováno v:
Seminars in nephrology. 19(2)
Immune-mediated nephritis is a common complication of systemic lupus erythematosus (SLE). It is now clear that multiple and independent mechanisms contribute to disease onset and pathogenesis, which may explain the remarkable phenotypic and histopath
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 161(1)
CSF-1 and TNF-alpha in the kidney of MRL-Fas(lpr) mice are proximal events that precede and promote autoimmune lupus nephritis, while apoptosis of renal parenchymal cells is a feature of advanced human lupus nephritis. In the MRL-Fas(lpr) kidney, inf
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 160(8)
IFN-gamma is capable of enhancing and limiting inflammation. Therefore, an increase in IFN-gamma in autoimmune MRL-Fas(lpr) mice could exacerbate or thwart renal injury. We have established a retroviral gene transfer approach to incite interstitial n
Autor:
V R, Kelley, K J, Moore
Publikováno v:
Experimental nephrology. 5(2)
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 157(1)
Mice with the MRL background have a genetic propensity for autoimmune lupus nephritis. The lpr mutation on the MRL, but not the C3H background, induces rapid and fatal renal injury in which macrophages (M phi) are prominent. We previously established
Publikováno v:
Journal of immunology (Baltimore, Md. : 1950). 157(1)
The lpr mutation on the MRL background accelerates autoimmune nephritis in which macrophage (M phi) accumulation is prominent. Renal disease is absent in other strains with lpr. TNF-alpha and CSF-1 are increased in the kidney of MRL-lpr mice with los