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Publication : Differential roles of osteopontin/Eta-1 in early and late lpr disease.

First Author  Weber GF Year  2001
Journal  Clin Exp Immunol Volume  126
Issue  3 Pages  578-83
PubMed ID  11737079 Mgi Jnum  J:73396
Mgi Id  MGI:2155046 Doi  10.1046/j.1365-2249.2001.01702.x
Citation  Weber GF, et al. (2001) Differential roles of osteopontin/Eta-1 in early and late lpr disease. Clin Exp Immunol 126(3):578-83
abstractText  The cytokine osteopontin (Eta-1) leads to macrophage-dependent polyclonal B-cell activation and is induced early in autoimmune prone mice with the lpr mutation, suggesting a significant pathogenic role for this molecule. Indeed, C57BL/6-Faslpr/lpr mice crossed with osteopontin-/- mice display delayed onset of polyclonal B-cell activation, as judged by serum immunoglobulin levels. In contrast, they are subject to normal onset, but late exacerbation of lymphoproliferation and evidence of kidney disease. These observations define two stages of Faslpr/lpr disease with respect to osteopontin-dependent pathogenesis that should be taken into account in the design of therapeutic approaches to the clinical disease.
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