Abstract
Gammadelta T cells are expanded in human IgA nephropathy and in a rat model of adriamycin (ADR)-induced nephropathy. Despite different diseases and species, these renal gammadelta T cells use a restricted set of gammadelta T cell receptor (TCR) genes. To explore whether this phenomenon of post injury expansion of gammadelta T cells occurs in autoimmune-mediated glomerulonephritis, we studied gammadelta TCR genes in Heymann nephritis (HN). Gammadelta T cells were increased in HN kidneys (p<0.001). These gammadelta T cells predominantly expressed Vgamma6/Vdelta1 genes and used canonical matching sequences previously seen in the other models of renal injury. Gammadelta T cells from the kidneys expressed high levels of TGF-beta, IL-4 and IL-5. The gammadelta T cells from both ADR-treated and HN kidneys expressed NKG2D, the NK cell-activating receptor. These results demonstrate that the majority of gammadelta T cells in the HN kidney use a canonical Vgamma6/Vdelta1 TCR--the gammadelta TCR previously described in the rat ADR-treated kidney. The restriction in gammadelta TCR seen in two completely different models of kidney injury and the expression of an innate activating molecule NKG2D suggests that the gammadelta T cells may be responding to tissue stress from injury and producing a regulatory response.
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