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Signaling in T Cells Prevents the Development of Experimental Glomerulonephritis1
*
Allergy Research Center,
Division of Nephrology Juntendo University School of Medicine, Tokyo, Japan
Anti-glomerular basement membrane (GBM) Ab-induced
glomerulonephritis (GN) at late stage is thought to be mediated by T
cells. However, signaling pathways of T cells that are involved in the
development of anti-GBM Ab-induced GN are unclear. We have recently
established transgenic mice expressing Smad7, an inhibitor of TGF-
signaling, in mature T cells, where signaling by TGF- was blocked
specifically in T cells. In this study, we showed that anti-GBM
Ab-induced GN was suppressed in several measures in the transgenic mice
including the severity of glomerular changes, proteinuria, renal
function, and CD4 T cell infiltration into the glomeruli without
down-regulation of CD62 ligand (CD62L) (L-selectin) expression on CD4 T
cells. Furthermore, treatment with the soluble fusion protein of CD62L
and IgG enhanced anti-GBM Ab-induced GN. These findings indicated
that blockade of TGF- signaling in T cells prevented the development
of anti-GBM Ab-induced GN. Because CD62L on T cells appears to be
inhibitory for the development of anti-GBM Ab-induced GN,
persistent expression of CD62L on CD4 T cells may explain, at least in
part, the suppression of anti-GBM Ab-induced GN in the transgenic
mice. Our findings suggest that the development of anti-GBM
Ab-induced GN requires TGF-/Smad signaling in T
cells.
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