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Expression of lymphotactin mRNA in experimental crescentic glomerulonephritis
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SUMMARYLymphotactin (LTN) is the sole member of C chemokine, the third subfamily of chemokines. LTN has been shown to be a chemoattractant specific for CD8+ cells and/or natural killer (NK) cells, and to be produced by CD8+ T cells, NK cells, and mast cells. However, there have been no reports describing its expression in clinical or experimental models of diseases so far. Since glomerular infiltration of CD8+ cells is prominent in an animal model of crescentic glomerulonephritis induced in WKY rats by an injection of anti-glomerular basement membrane antibody, we investigated the gene expression of LTN in this model. LTN mRNA was not detected in normal glomeruli but was detected at 0.5 h after the antibody injection, which detection preceded the infiltration of CD8+ cells. The expression of LTN mRNA peaked on day 3 and decreased thereafter. We next studied the expression of LTN mRNA in cultured glomerular and vascular cells, and found that glomerular mesangial and vascular endothelial cells could express LTN mRNA when stimulated with IL-1β. These results indicate that the gene expression of LTN is enhanced in the animal model of glomerulonephritis and that intrinsic renal cells are the potential source of the gene expression of LTN in the kidney.
Oxford University Press (OUP)
Title: Expression of lymphotactin mRNA in experimental crescentic glomerulonephritis
Description:
SUMMARYLymphotactin (LTN) is the sole member of C chemokine, the third subfamily of chemokines.
LTN has been shown to be a chemoattractant specific for CD8+ cells and/or natural killer (NK) cells, and to be produced by CD8+ T cells, NK cells, and mast cells.
However, there have been no reports describing its expression in clinical or experimental models of diseases so far.
Since glomerular infiltration of CD8+ cells is prominent in an animal model of crescentic glomerulonephritis induced in WKY rats by an injection of anti-glomerular basement membrane antibody, we investigated the gene expression of LTN in this model.
LTN mRNA was not detected in normal glomeruli but was detected at 0.
5 h after the antibody injection, which detection preceded the infiltration of CD8+ cells.
The expression of LTN mRNA peaked on day 3 and decreased thereafter.
We next studied the expression of LTN mRNA in cultured glomerular and vascular cells, and found that glomerular mesangial and vascular endothelial cells could express LTN mRNA when stimulated with IL-1β.
These results indicate that the gene expression of LTN is enhanced in the animal model of glomerulonephritis and that intrinsic renal cells are the potential source of the gene expression of LTN in the kidney.
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