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4/V
1 T Cells in an Adriamycin-Induced Progressive Renal Failure Model1
*
Center for Kidney Research, Royal Alexandra Hospital for Children, Westmead, Sydney, Australia; and
Second Department of Internal Medicine, Kyushu University, Fukuoka, Japan
We have previously reported an infiltration of renal interstitial
T cells in Adriamycin-induced progressive glomerulosclerosis in
the rat kidney. The TCR repertoire and sequences used by these T
cells have now been studied. Two injections of Adriamycin 14 days apart
caused segmental glomerulosclerosis, massive interstitial infiltration
of mononuclear cells, and end-stage renal failure. Flow cytometry of
lymphocyte subpopulations with Abs to CD3, the TCR, and the
TCR showed that T cells as a proportion of
CD3+ cells were increased in Adriamycin-treated kidneys
(8.5 ± 5.4%), but not in lymph nodes (1.3 ± 0.4%). A
semiquantitative score of glomerular damage (r =
0.65; p < 0.01) and creatinine
(r = 0.62; p < 0.01)
correlated significantly with the presence of T cells. TCR V
repertoire analysis by RT-PCR and Southern blotting showed that V2
was the dominant subfamily in lymph nodes, whereas V4 became the
predominant subfamily in advanced stages of the rat Adriamycin-treated
kidney. Sequencing of the V4-J junctional region showed an
invariant sequence. The amino acid sequence of the junctional region of
the V4 TCR was the same as the reported mouse canonical V4 TCR
sequence. Analysis of the kidney V repertoire showed dominant
expression of V1, and sequencing again revealed the selective
expression of a canonical V1 gene. Semiquantitative RT-PCR for
cytokine gene expression showed that T cells from the kidneys
expressed TGF-, but not IL-4, IL-10, or IFN-. These results
suggest that the predominant T cells in the Adriamycin kidney
use an invariant V4/V1 receptor.
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