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editorial
. 2012 Mar;91(3):353–355. doi: 10.1189/jlb.1011495

Table 1. Top Four NET Queries in My Queue.

  1. What are the mechanisms for NETs formation?
    • —What are the relationships among NETs formation and autophagy, mitochondrial DNA release, and histone citrullation?
    • —Are all NETs the same? What mechanisms operate in cells that constitutively lack MPO (e.g., chicken heterophils)?
  2. What is the fate of microbes trapped in NETs in vitro?
    • —Are organisms trapped and thereby immobilized for attack by other elements of the immune system—soluble and cellular?
    • —Are organisms killed in situ by NETs alone? If so, how? If killing is MPO-dependent, what are the sources of H2O2?
  3. Are NETs generated in vivo during infection?
    • —Do NETs appear late in infection after neutrophils are exhausted and dead?
    • —Are NETs present in abscesses or areas where large numbers of dead neutrophils are generated?
  4. What is the contribution of NETs-mediated antimicrobial action to overall host defense?
    • —In the presence of intact phagocytes, what fraction of microbial killing or bacteriostasis can be attributed NETs?
    • —How do the signals that promote formation of NETs derail those that initiate events that promote apoptosis?