Abstract
Objective. To examine the role played by E-selectin in bystander IgM-mediated modification of glomerular lesions in experimental lupus nephritis. Methods. Experimental lupus SCID mice were induced by an intraperitoneal injection of clone 7B6.8, which was derived from a MRL/lpr mouse and shown to induce wire-loop type glomerular lesions. Mice were subsequently administered clone Sp6, a non-nephritogenic IgM antibody- producing hybridoma. E-selectin expression was then evaluated in glomeruli showing histopathological conversion of lesions from wire-loop-like to a cell-proliferative form. We also investigated the effects of a circulating soluble form of E-selectin (sE-selectin) on the modification of glomerular lesions in this lupus model. Results. In experimental lupus mice, glomerular E-selectin expression significantly increased during the conversion from wire-loop-like glomerular lesions to a cell-proliferative type mediated by a non-nephritogenic bystander IgM antibody in presence of a nephritogenic antibody. Intraglomerular infiltration of CD68 + macrophages correlated significantly with the glomerular level of E-selectin expression. In addition, overexpression of circulating sE-selectin significantly suppressed conversion to cell-proliferative glomerular lesions and glomerular macrophage infiltration in these lupus model mice. Conclusions. The histopathological modification of lupus nephritis by non-nephritogenic bystander IgM antibodies is associated in part with glomerular E-selectin expression.
Original language | English |
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Pages (from-to) | 808-815 |
Number of pages | 8 |
Journal | Modern Rheumatology |
Volume | 24 |
Issue number | 5 |
DOIs | |
Publication status | Published - 2014 Sep |
Keywords
- E-selectin
- Histopathology
- IgM antibody
- Lupus nephritis
- Nephritogenic antibody
ASJC Scopus subject areas
- Rheumatology