BACKGROUND: We previously reported that glomerulonephritis associated with Staphylococcus aureus infection (SAGN) showed an increased usage of T cell receptor Vbeta 5.3 and 8 in peripheral lymphocytes and mesangial IgA and IgG depositions. To elucidate the immunological mechanisms and pathogenesis of IgA nephropathy, we analyzed the usage of TCR Vbeta in both peripheral blood lymphocytes (PBLs) and renal infiltrating T cells from IgA-N patients. METHODS: In 38 patients with IgA nephropathy and controls, the usage of TCR Vbeta in PBLs were analyzed using monoclonal antibodies against Vbeta 3.1, Vbeta 5.1, Vbeta 5.2 + 5.3, Vbeta 5.3, Vbeta 6.7, Vbeta 8, Vbeta 12.1, and Vbeta 13.1 + 13.3 with three-color flow cytometry. Furthermore, we examined immunohistochemically renal biopsy specimens using antibodies against Vbeta 5.3 and Vbeta 8. RESULTS: The percentages of DR+CD4+CD8- cells, CD45RO+CD4+ cells, and CD45RO+CD4+DR+ cells in PBLs from IgA nephropathy were significantly higher than controls. The percentages of TCR Vbeta 5.3 positive cells and TCR Vbeta 8 positive cells in PBLs from patients were 1.3 +/- 0.1 and 3.1 +/- 0.2%, and both were significantly higher than controls. The percentage of renal interstitial TCR Vbeta 5.3 expression was significantly higher than that in PBLs. However, there was no significant difference between the TCR Vbeta 8 expression in the interstitium and that in PBLs. CONCLUSIONS: TCR Vbeta 5.3 and 8 usage and broad CD4+ T cell activation have occurred in IgA nephropathy. These changes were similar but weak compared with formerly reported SAGN. Copyright 2002 S. Karger AG, Basel
BACKGROUND: We previously reported that glomerulonephritis associated with Staphylococcus aureus infection (SAGN) showed an increased usage of T cell receptor Vbeta 5.3 and 8 in peripheral lymphocytes and mesangial IgA and IgG depositions. To elucidate the immunological mechanisms and pathogenesis of IgA nephropathy, we analyzed the usage of TCR Vbeta in both peripheral blood lymphocytes (PBLs) and renal infiltrating T cells from IgA-N patients. METHODS: In 38 patients with IgA nephropathy and controls, the usage of TCR Vbeta in PBLs were analyzed using monoclonal antibodies against Vbeta 3.1, Vbeta 5.1, Vbeta 5.2 + 5.3, Vbeta 5.3, Vbeta 6.7, Vbeta 8, Vbeta 12.1, and Vbeta 13.1 + 13.3 with three-color flow cytometry. Furthermore, we examined immunohistochemically renal biopsy specimens using antibodies against Vbeta 5.3 and Vbeta 8. RESULTS: The percentages of DR+CD4+CD8- cells, CD45RO+CD4+ cells, and CD45RO+CD4+DR+ cells in PBLs from IgA nephropathy were significantly higher than controls. The percentages of TCR Vbeta 5.3 positive cells and TCR Vbeta 8 positive cells in PBLs from patients were 1.3 +/- 0.1 and 3.1 +/- 0.2%, and both were significantly higher than controls. The percentage of renal interstitial TCR Vbeta 5.3 expression was significantly higher than that in PBLs. However, there was no significant difference between the TCR Vbeta 8 expression in the interstitium and that in PBLs. CONCLUSIONS: TCR Vbeta 5.3 and 8 usage and broad CD4+ T cell activation have occurred in IgA nephropathy. These changes were similar but weak compared with formerly reported SAGN. Copyright 2002 S. Karger AG, Basel