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Interleukin-9 is a major anti-apoptotic factor for thymic lymphomas
J C Renauld1, A Vink, J Louahed
1Ludwig Institute for Cancer Research, Brussels, Belgium.
Blood
|March 1, 1995
Summary
Interleukin-9 (IL-9) inhibits apoptosis and maintains proliferation in mouse thymic lymphomas treated with dexamethasone (DEX). This suggests distinct cytokine-driven regulatory mechanisms for lymphoma cell growth and death.
Area of Science:
- Immunology
- Cell Biology
- Oncology
Background:
- Interleukin-9 (IL-9) was previously shown to stimulate mouse thymic lymphoma proliferation in vitro.
- Thymic lymphomas can be induced to undergo apoptosis by dexamethasone (DEX).
Purpose of the Study:
- To investigate the role of IL-9 and other cytokines in regulating apoptosis and proliferation of mouse thymic lymphomas.
- To determine if cytokine effects on proliferation and apoptosis are distinct in thymic lymphoma cell lines.
Main Methods:
- Treatment of factor-independent and factor-dependent mouse thymic lymphoma cell lines with various interleukins (IL-2, IL-4, IL-6, IL-7, IL-9, IL-10) and dexamethasone (DEX).
- Assessment of cell proliferation and inhibition of DEX-induced apoptosis.
- Comparison of the effects of IL-2 and IL-9 on proliferation and apoptosis in a factor-dependent cell line.
Main Results:
- IL-9 was a potent inhibitor of DEX-induced apoptosis and maintained proliferation in most tested thymic lymphoma cell lines.
- IL-4 also protected against apoptosis and maintained proliferation, while IL-6 showed weaker protection, and IL-2, IL-7, and IL-10 were largely inactive.
- In a factor-dependent cell line, IL-2 was a stronger inducer of proliferation, whereas IL-9 was more effective at inhibiting apoptosis.
Conclusions:
- Cytokines, particularly IL-9 and IL-4, play a significant role in protecting thymic lymphomas from apoptosis induced by DEX.
- These cytokines can also maintain lymphoma cell proliferation in the presence of DEX.
- The findings suggest that proliferation and apoptosis in thymic lymphomas are regulated by distinct mechanisms that can be differentially modulated by cytokines.