| Autor: |
Bailey DP; Department of Biology, Virginia Commonwealth University, Richmond, 23284-2012, USA., Kashyap M, Bouton LA, Murray PJ, Ryan JJ |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of leukocyte biology [J Leukoc Biol] 2006 Sep; Vol. 80 (3), pp. 581-9. Date of Electronic Publication: 2006 Jul 07. |
| DOI: |
10.1189/jlb.0405201 |
| Abstrakt: |
Interleukin (IL)-10 is a potent immunoregulatory cytokine capable of inhibiting the inflammatory response. As mast cells and macrophages are central effectors of inflammation, we investigated the effects of IL-10 on mast cell and macrophage development from mouse bone marrow progenitors. Bone marrow cells were cultured in IL-3 + stem cell factor (SCF), giving rise to mixed populations of mast cells and macrophages. The addition of IL-10 greatly decreased the expansion of bone marrow progenitor cells through a mechanism requiring signal tranducer and activator of transcription-3 expression. The inhibitory effects were a result of the induction of apoptosis, which occurred with caspase-3 activation and reduced mitochondrial membrane potential. Supporting a role for the mitochondrion, bone marrow cells from p53-deficient or Bcl-2 transgenic mice were partly resistant to the effects of IL-10. Further, IL-10 decreased Kit receptor expression and inhibited survival signaling by SCF or IL-3. These data indicate that IL-10 induces an intrinsic, mitochondrial apoptosis cascade in developing mast cells and macrophages through mechanisms involving blockade of growth factor receptor function. The ability of IL-10 to inhibit survival could support immune homeostasis by dampening inflammatory responses and preventing chronic inflammation. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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