T cells have long been suspected to contribute to glomerulonephritis not only as helpers for antibody-producing B cells, but also as immune effector cells. Recent evidence has substantiated this hypothesis, by identifying tubulointerstitial dendritic cells (DCs) as crucial interaction partners. Kidney DCs capture glomerular antigens released for example by cytotoxic CD8(+) T cells and present them to infiltrating CD4(+) T helper cells. This cross-talk results in the production of proinflammatory cytokines and chemokines that recruit and activate further immune effector cells. Such immunocytes are the main components of the well-known tubulointerstitial mononuclear infiltrate characteristic of progressive renal disease. These findings indicate that effector T cell dysregulation by intrarenal DCs and by the chemokines they produce represents a hitherto unknown mechanism by which glomerular damage can cause chronic tubulointerstitial inflammation.
