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Recombinant interleukin-16 selectively modulates surface receptor expression and cytokine release in macrophages and
E Hermann1, E Darcissac, T Idziorek
1Institut Pasteur de Lille, INSERM U167, Lille, France.
Insights
Interleukin-16 (IL-16) modulates antigen-presenting cells, affecting CD4 receptor expression and chemokine pathways. This research explores IL-16
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Interleukin-16 (IL-16) is a CD4 receptor ligand known to modulate T-lymphocyte function and inhibit HIV-1 replication.
- Antigen-presenting cells (APCs), such as macrophages and dendritic cells, express CD4, are susceptible to HIV-1, and play key immune roles.
Purpose of the Study:
- To evaluate the effect of recombinant IL-16 (rIL-16) on receptor expression and cytokine release in monocyte-derived macrophages (MDM) and dendritic cells (MDDC).
- To investigate IL-16's role in modulating APC activity and its potential relevance for protecting HIV-1 reservoir cells.
Main Methods:
- Treatment of MDM and MDDC cultures with recombinant IL-16 (rIL-16).
- Analysis of surface marker expression (CD4, CD25, CD80, CD86, CD83) using flow cytometry.
- Quantification of chemokine receptor (CCR5, CXCR4) gene expression via RT-PCR.
- Measurement of cytokine and chemokine release in culture supernatants.
Main Results:
- In MDM, rIL-16 up-regulated CD25 and CD80, while down-regulating CD4 and CD86. It also significantly reduced CCR5 and CXCR4 gene expression.
- In MDDC, rIL-16 significantly up-regulated CD25 and CD83, with minimal impact on CD4, CD80, and CD86. Chemokine receptor expression changes were transient and less pronounced.
- Distinct profiles of released cytokines/chemokines were observed between rIL-16-stimulated MDM and MDDC.
Conclusions:
- Recombinant IL-16 significantly modulates surface receptor expression and chemokine receptor gene expression in monocyte-derived macrophages.
- IL-16 also influences receptor expression in monocyte-derived dendritic cells, though to a lesser extent regarding chemokine receptors.
- These findings highlight IL-16's role in regulating APC function and suggest potential implications for HIV-1 infection control.
Abstract:
Interleukin-16 (IL-16), a natural ligand for the CD4 receptor, has been found to modulate T-lymphocyte function and to inhibit human immunodeficiency virus type 1 (HIV-1) replication. Antigen-presenting cells (APC), including macrophages and dendritic cells, are known to express functional surface CD4 molecules, to be susceptible to HIV-1 infection and to play a critical role in different immune processes. Therefore, we evaluated the ability of recombinant IL-16 (rIL-16) to regulate receptor expression and cytokine release in monocyte-derived macrophages (MDM) and monocyte-derived dendritic cells (MDDC). Recombinant IL-16 was found to up-regulate CD25 and CD80 but to down-regulate CD4 and CD86 surface expression in MDM cultures. However, no change could be observed on the level of CD4, CD80 and CD86 expression in IL-16-stimulated MDDC, although a significant up-regulation of CD25 and CD83 was consistently detected. Furthermore, the level of gene expression of the chemokine receptors CCR5 and CXCR4 was significantly reduced in rIL-16-treated MDM and costimulation with IL-2 did not modify the activity of the recombinant cytokine. The effects on chemokine receptor gene expression were less evident in MDDC and only a transient down-regulation of weak intensity could be detected following stimulation with rIL-16. Analysis of supernatants from rIL-16-stimulatedcultures revealed a different profile of released cytokines/chemokines among the two cell populations studied. These findings establish an important role for IL-16 in modulating the activity of APC and may have relevance regarding the protection of reservoir cells against HIV-1 infection.
