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Updated: Aug 14, 2026

Isolation and Activation of Murine Lymphocytes
Published on: October 30, 2016
Activation of human monocytes by interleukin 2: role of T lymphocytes
1Forschungsinstitut Borstel, Department of Immunology and Cell Biology, FRG.
Insights
Interleukin 2 (IL2) primes human monocytes for enhanced reactive oxygen species secretion via Fc-gamma receptors, but requires T-cell interaction. This IL2-driven monocyte and T-cell cooperation boosts Fc-gamma R-mediated activity.
Area of Science:
- Immunology
- Cell Biology
Background:
- Interleukin 2 (IL2) is a key cytokine in immune regulation.
- Monocytes play a crucial role in innate immunity, including the respiratory burst.
- Fc-gamma receptors (Fc-gamma R) on monocytes mediate phagocytosis and inflammatory responses.
Purpose of the Study:
- To investigate the effect of IL2 on human monocyte reactive oxygen species (ROS) secretion.
- To determine the role of T cells in IL2-mediated monocyte activation.
- To elucidate the mechanisms underlying IL2-induced monocyte priming and activation.
Main Methods:
- Chemiluminescence (CL) assays were used to measure ROS production.
- Highly purified (hp) human monocytes were used, with and without co-culture of T cells.
- Monoclonal antibodies were employed to block specific cytokine and receptor interactions.
Main Results:
- IL2 alone did not directly enhance ROS production in hp monocytes.
- Co-culture of hp monocytes with T cells was necessary for IL2 to enhance Fc-gamma R-mediated ROS secretion.
- IL2 pretreatment primed monocytes, leading to enhanced Fc-gamma R-mediated CL response upon subsequent T-cell co-culture.
- IL2-induced monocyte activation and MAF secretion were dependent on IL2 receptor interaction.
Conclusions:
- IL2-driven monocyte-T cell interaction enhances Fc-gamma R-mediated monocytic respiratory burst activity.
- IL2 primes monocytes for enhanced responses, dependent on IL2 receptor signaling.
- Soluble monocyte activating factor (MAF) activity is secreted, but interferon-gamma (IFN-gamma) was not detected in IL2-stimulated T-cell dependent monocyte cultures.
Abstract:
The effect of interleukin 2 (IL2) on the capability of human monocytes to secrete reactive oxygen species triggered via Fc-gamma receptor (Fc-gamma R) function had been investigated by measurement of chemiluminescence (CL). IL 2 did not activate highly purified (hp) monocytes to respond to Fc-gamma R mediated phagocytic stimulation with an enhanced respiratory burst activity unless low numbers of T cells had been co-cultured with hp monocytes. Supernatants from IL 2 treated PBMC contained interferon-gamma (IFN-gamma) and monocyte activating factor (MAF) activity. The secretion of both cytokine activities was strongly enhanced by cooperative function of monocytes. The correlation of IL 2 induced secretion of IFN-gamma and MAF activity was striking, however, monoclonal antibody (mAb) anti-human IFN-gamma failed to abrogate IL 2 stimulated and lymphocyte dependent monocyte activation. Although IL 2 had no direct monocyte activating effect, pretreatment of hp monocytes with IL 2 led to monocyte priming: subsequent co-culture with autologous control T cells enhanced the monocyte Fc-gamma R mediated CL response. The priming of monocytes by IL 2 was dependent on the interaction of IL 2 with the monocytic IL 2 receptor as shown by inhibition experiments with anti IL 2 R monoclonal antibody. Thus the IL 2 driven monocyte/T-cell interaction leads to an increased Fc-gamma R mediated monocytic respiratory burst activity and to the secretion of a soluble MAF activity, but there were no detectable amounts of IFN-gamma.
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