The cytokine interferon-γ (IFN-γ), when released by lymphocytes, augments the capacity of macrophages and other host cells to kill certain intracellular protozoa, bacteria, and viruses (1–3). However, the function of most of the hundreds of genes induced by IFN-γ is unknown, and biochemical mechanisms of pathogen inactivation are incompletely understood. On page 296 of this issue, Gaudet et al. (4) identify an effector mechanism in the human immune system: production of IFNγ–induced apolipoprotein L3 (APOL3) in epithelial cells, endothelial cells, and fibroblasts that acts like a detergent, extracting lipids from membranes of bacteria in the cytosol, killing the bacteria. Not only does APOL3 dissolve a biophysical boundary—the bacterial inner membrane—but the findings of Gaudet et al. help dissolve conceptual boundaries about the composition of the immune system.
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