1. Immunology and Inflammation
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Lung Disease: The soot of all evil

  1. Derek W Russell
  2. J Edwin Blalock  Is a corresponding author
  1. University of Alabama at Birmingham, United States
Cite this article as: eLife 2015;4:e11709 doi: 10.7554/eLife.11709
1 figure


Nanocarbon black triggers perpetual inflammation in the lung.

Nanoparticles of carbon black are consumed by antigen-presenting cells, such as human myeloid dendritic cells, where they lead to DNA breaks. This, in turn, initiates the activation of a complex of proteins called the inflammasome, which includes the Caspase-1 protein (Taniguchi and Sagara, 2007). The activated inflammasome leads to the cleavage of Pro-IL1β to make a mature signal protein called IL-1β, while also initiating processes that will lead to the death of the cell. The mature IL-1β causes upregulation of several inflammatory pathways, including the increased transcription of IL-6. These cytokines then act together to trigger T lymphocytes to become T helper 17 (TH17) cells. These cells produce the inflammatory cytokine IL-17, which has been implicated in chronic obstructive pulmonary disease. When the antigen-presenting cell dies, the nanoparticles are released to be taken up by another generation of antigen-presenting cells, which lead to another cycle of inflammation. IL = interleukin; ASC = Adaptor Protein Apoptosis-Associated Speck-Like Protein Containing CARD.

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