Early events in spontaneous neutrophil apoptosis

  • D. Scheel-Toellner
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.
  • K.-Q. Wang
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.
  • P.R. Webb
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.
  • S.H. Wong
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.
  • R. Craddock
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.
  • L.K. Assi
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.
  • M. Salmon
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.
  • J.M. Lord
    MRC Centre for Immune Regulation, University of Birmingham Medical School, Edgbaston, Birmingham B15 2TT, U.K.

抄録

<jats:p>Neutrophils are very abundant, short-lived leucocytes and their death by apoptosis is central to homoeostasis and the resolution of inflammation, yet the trigger for apoptosis is still a topic of debate. Depolarization of the mitochondrial membrane has been supposed to initiate neutrophil spontaneous apoptosis, as neutrophils gradually lose the anti-apoptotic protein Mcl-1 and Bax translocates and inserts into the mitochondrial membrane. However, other reports show that caspase 8 is required for neutrophil apoptosis, suggesting the involvement of DR (death receptor) signalling. As DR ligation is not required for neutrophil apoptosis, this raises the intriguing possibility that activation of caspase 8 during neutrophil apoptosis occurs via a novel mechanism. In the present paper, we discuss the current evidence for mechanisms occurring in neutrophil apoptosis, which could trigger DR signalling in the absence of DR ligation.</jats:p>

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