Biologic control of the tumor necrosis factor and interleukin-1 signaling cascade.
It is clear that activation of the proinflammatory cytokine cascade is both the cause and the consequence of renal injury. Recently, it has been appreciated that a rich network of signaling pathways contributes to modulation of tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) bioactivity, both in vitro and in vivo. Insight into the checks and balances that intervene or temper endogenous cytokine effector mechanisms has arisen from an explosion of new information on the cell biology of proinflammatory cytokines. Novel mechanisms of cytokine regulation are currently being described and hold promise for therapeutic potential: soluble cytokine receptors, endogenous receptor antagonists, and anti-inflammatory cytokines such as IL-4, IL-10, and IL-13.
Stewart
R J
RJ
Renal Division, St Michael's Hospital, Toronto, Ontario, Canada.
Marsden
P A
PA
D000818:Animals; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000502:physiology*; D016753:Interleukin-10 / Q000502:physiology; D018793:Interleukin-13 / Q000502:physiology; D007674:Kidney Diseases / Q000503:physiopathology; D017472:Receptors, Interleukin-1 / Q000502:physiology; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D012795:Sialoglycoproteins / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D018793:Interleukin-13; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10