Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 11, Pages 6553-6561Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1100478
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Funding
- NIGMS NIH HHS [R01 GM036387, R01 GM036387-22, R01 GM036387-23] Funding Source: Medline
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Apoptotic cell death is important for embryonic development, immune cell homeostasis, and pathogen elimination. Innate immune cells also undergo a very rapid form of cell death termed pyroptosis after activating the protease caspase-1. The hemichannel pannexin-1 has been implicated in both processes. In this study, we describe the characterization of pannexin-1-deficient mice. LPS-primed bone marrow-derived macrophages lacking pannexin-1 activated caspase-1 and secreted its substrates IL-1 beta and IL-18 normally after stimulation with ATP, nigericin, alum, silica, flagellin, or cytoplasmic DNA, indicating that pannexin-1 is dispensable for assembly of caspase-1-activating inflammasome complexes. Instead, thymocytes lacking pannexin-1, but not the P2X7R purinergic receptor, were defective in their uptake of the nucleic acid dye YO-PRO-1 during early apoptosis. Cell death was not delayed but, unlike their wild-type counterparts, Panx1(-/-) thymocytes failed to recruit wild-type peritoneal macrophages in a Transwell migration assay. These data are consistent with pannexin-1 liberating ATP and other yet to be defined find me signals necessary for macrophage recruitment to apoptotic cells. The Journal of Immunology, 2011, 186: 6553-6561.
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