Leukocyte-derived interleukin-1beta interacts with renal interleukin-1 receptor I to promote renal tumor necrosis factor and glomerular injury in murine crescentic glomerulonephritis.

The involvement of proinflammatory cytokines interleukin (IL)-1 and tumor necrosis factor (TNF) in crescentic glomerulonephritis (GN) is well established. Recently the requirement of intrinsic renal cell participation via their production of TNF in crescentic GN was demonstrated. The current studies address the relative contributions of leukocyte and intrinsic renal cell-derived IL-1beta in the induction of TNF production and glomerular injury by studying bone marrow chimeric mice.

Contributions of IL-1beta and IL-1alpha to crescentic glomerulonephritis in mice.

ABSTRACT. Interleukin-1 (IL-1) is a pleiotropic proinflammatory cytokine with two distinct isoforms (IL-1alpha and IL-1beta) that signal through the same IL-1 type I receptor (IL-1RI). Contributions of IL-1beta have been demonstrated in human and experimental proliferative glomerulonephritis (GN), but the involvement of IL-1alpha has received little attention.