In particular, in rapidly progressive or crescentic glomerulonephritis (RPGN), infiltrating CD4+ effector T cells of the Th1 and Th17 types release proinflammatory cytokines that directly promote tissue damage and stimulate chemokine production by renal resident cells, leading to the recruitment of additional leukocyte subsets and the subsequent loss of renal function, while the role of CD8+ T cells in RPGN remains controversial (3–7). This evidence concerns the gene CD4 and crescentic glomerulonephritis.