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Interleukin-2 inhibits growth of fibroblasts derived from human bone marrow
D MacDonald1, J A Adams, D McCarthy
1Department of Haematology, Westminster Hospital, London, UK.
Abstract:
The adherent layer that forms in human bone marrow suspension cultures contains fibroblast colonies which arise from colony-forming cells (CFU-F). We have demonstrated that recombinant interleukin-2 (r-IL2) inhibits growth of CFU-F by preventing their entry into S phase. This inhibition is not mediated by gamma-interferon, nor by T lymphocytes, and can be abrogated by anti-IL2 receptor antibody. r-IL2 may influence haematopoiesis by its effect on bone marrow CFU-F.
Insights
Recombinant interleukin-2 (r-IL2) stops fibroblast colony-forming cells (CFU-F) in bone marrow from growing by blocking their cell cycle entry. This finding suggests r-IL2 impacts human hematopoiesis through its effects on bone marrow CFU-F.
Area of Science:
- Hematology
- Cell Biology
- Immunology
Background:
- Bone marrow suspension cultures form an adherent layer containing fibroblast colonies.
- These colonies originate from colony-forming cells (CFU-F).
Purpose of the Study:
- To investigate the effect of recombinant interleukin-2 (r-IL2) on the growth of CFU-F in human bone marrow cultures.
- To elucidate the mechanism by which r-IL2 influences CFU-F proliferation.
Main Methods:
- Human bone marrow suspension cultures were utilized.
- The impact of r-IL2 on CFU-F growth and cell cycle progression was assessed.
- Experiments included the use of anti-IL2 receptor antibody and assessments for gamma-interferon and T lymphocytes.
Main Results:
- Recombinant interleukin-2 (r-IL2) was found to inhibit the growth of CFU-F.
- This inhibition occurs by preventing CFU-F from entering the S phase of the cell cycle.
- The inhibitory effect was not mediated by gamma-interferon or T lymphocytes and could be reversed by an anti-IL2 receptor antibody.
Conclusions:
- r-IL2 directly inhibits the proliferation of bone marrow CFU-F.
- r-IL2 influences hematopoiesis through its inhibitory action on bone marrow CFU-F.
- The mechanism involves blocking cell cycle progression into S phase, independent of T cells or gamma-interferon.