To uncover the inflammatory pathways involved in cell injury and death, Kenneth Rock at the University of Massachusetts and colleagues injected necrotic cells into mice deficient in various toll-like receptors and found that neutrophilic inflammatory response was not significantly reduced. 1 Using the same strategy in interleukin-1 (IL-1) receptor-deficient mice, along with mice with induced liver damage in situ, they found that the IL-1 pathway was required for the inflammatory response triggered by dead and injured cells.













