IL-6 attenuates apoptosis, while neither IL-6 nor IL-10 affect the numbers or protease phenotype of fetal liver-derived human mast cells
Article first published online: 20 DEC 2001
Clinical & Experimental Allergy
Volume 31, Issue 7, pages 1077–1085, July 2001
How to Cite
Kambe, M., Kambe, N., Oskeritzian, C. A., Schechter, N. and Schwartz, L. B. (2001), IL-6 attenuates apoptosis, while neither IL-6 nor IL-10 affect the numbers or protease phenotype of fetal liver-derived human mast cells. Clinical & Experimental Allergy, 31: 1077–1085. doi: 10.1046/j.1365-2222.2001.01126.x
- Issue published online: 20 DEC 2001
- Article first published online: 20 DEC 2001
- Submitted 5 October 2000; revised 18 December 2000; accepted 22 January 2001.
- mast cells;
- stem cell factor;
Background The combination of recombinant human stem cell factor (rhSCF), rh interleukin (IL)-6 and rhIL-10 was reported to be optimal for mast cell development from cord blood progenitors and to induce chymase expression in all such mast cells earlier in their development than tryptase.
Objective The effects of rhIL-6 and rhIL-10 in various combinations on the rhSCF-dependent development of human mast cells from fetal liver progenitors were examined in serum-free media.
Methods Dispersed fetal liver cells were cultured in serum-free AIM-V medium with rhSCF alone, or with combinations of rhIL-6 and rhIL-10. Tryptase and chymase expression, surface Kit expression, metachromasia with toluidine blue and apoptosis were measured.
Results Neither rhIL-6 nor rhIL-10 nor the two interleukins together, when included from day 0 of culture, affected the number or protease phenotype of mast cells at 1 or 3 weeks. Expression of tryptase paralleled the appearance of metachromasia and surface Kit, both of which preceded chymase expression, regardless whether a rabbit polyclonal or mouse monoclonal anti-chymase antibody preparation was used. On the other hand, rhIL-6 markedly attenuated baseline levels of apoptosis in the presence of rhSCF as well as apoptosis occurring after withdrawal of rhSCF, whereas rhIL-10 had no effect.
Conclusion RhIL-6 protected fetal liver-derived mast cells from apoptosis, particularly after withdrawal of rhSCF, but neither rhIL-6 nor rhIL-10 nor the combination of these interleukins affected the numbers or protease phenotype of these mast cells.