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Inhibitory effect of interleukin-10 on human leukocyte interferon-alpha production by Sendai virus
X X Zhao1, M J Liao, A Rashidbaigi
1Interferon Sciences Inc, New Brunswick, NJ 08901-3605, USA.
Cytokines, Cellular & Molecular Therapy
|April 29, 1998
Summary
Interleukin-10 (IL-10) significantly inhibits interferon-alpha (IFN-alpha) production by human leukocytes stimulated with Sendai virus. This cytokine-mediated regulation occurs early in the immune response at the transcriptional level.
Area of Science:
- Immunology
- Molecular Biology
- Virology
Background:
- Human peripheral blood leukocytes (hPBL) produce interferon-alpha (IFN-alpha) upon stimulation with Sendai virus.
- Interferon-alpha plays a crucial role in the innate immune response to viral infections.
Purpose of the Study:
- To investigate the effect of Interleukin-10 (IL-10) on Sendai virus-induced IFN-alpha production in hPBL.
- To elucidate the mechanism and stage of IL-10-mediated regulation of IFN-alpha synthesis.
Main Methods:
- hPBL were treated with Sendai virus in the presence or absence of varying concentrations of human recombinant IL-10.
- IFN-alpha production was quantified.
- The effect of anti-IL-10 antibodies was assessed.
- IFN-alpha mRNA levels were analyzed using quantitative methods.
Main Results:
- IL-10 significantly inhibited IFN-alpha production in a dose-dependent manner, with an effective dose (ED50) of approximately 5 ng/ml.
- Inhibition occurred early in the Sendai virus induction process.
- The inhibitory effect was specific to IL-10 and could be blocked by anti-IL-10 antibodies.
- IL-10 was found to inhibit IFN-alpha mRNA accumulation, indicating transcriptional regulation.
Conclusions:
- Leukocyte production of IFN-alpha is a tightly regulated process.
- IL-10 acts as a negative regulator of IFN-alpha production during the early stages of viral infection response.
- Cytokines like IL-10 play a significant role in modulating the immune response to pathogens.
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