Crescentic glomerulonephritis can be induced in rodents by injection of het
erologous antibodies against the glomerular basement membrane. There is evi
dence that glomerular inflammation in that model represents a delayed-type
hypersensitivity response to the heterologous immunoglobulin, whereas the a
ntibody response is not important. The aim of the present study was to test
this hypothesis. Delayed-type hypersensitivity is mediated by T cells with
the Th1 phenotype. We compared mice immunized with rabbit immunoglobulin G
in complete Freund's adjuvant or in incomplete Freund's adjuvant, producin
g, respectively, Th1- or Th2-biased responses to the antigen. Intravenous i
njection of rabbit antimouse glomerular basement membrane serum provoked pr
oteinuria, infiltration with T cells and macrophages, as well as profound h
istological damage in the group treated with complete Freund's adjuvant. Th
ere was no evidence of glomerulonephritis in the group which received incom
plete Freund's adjuvant. Deposits of mouse IgG along the glomerular basemen
t membrane were similar in both groups. Thus, a Th1 response appears to be
essential for the induction of glomerulonephritis in this model.