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Updated: Aug 11, 2026

In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
Published on: October 16, 2013
Involvement of CD4 in interleukin-6 secretion by U937 monocytic cells stimulated with the lectin jacalin
M Taimi1, J Dornand, M Nicolas
1INSERM U65, Université Montpellier II, Sciences et Techniques du Languedoc, France.
Insights
Jacalin lectin stimulates interleukin-6 (IL-6) production in CD4+ monocyte/macrophage cells. This effect is CD4-dependent, as shown by inhibition with anti-CD4 agents and lack of response in CD4-negative cells.
Area of Science:
- Immunology
- Cell Biology
- Virology
Background:
- Jacalin lectin interacts with the CD4 molecule and inhibits HIV infection in T lymphocytes.
- CD4 molecule is also expressed on cells of the monocyte/macrophage lineage.
Purpose of the Study:
- To investigate the effect of jacalin on CD4+ cells of the monocyte/macrophage lineage.
- To determine the role of the CD4 molecule in jacalin-induced cellular responses.
Main Methods:
- U937 promyelomonocytic cells were differentiated into monocyte/macrophage lineage using retinoic acid (RA)/vitamin D3 (VD) or phorbol myristate acetate (PMA).
- CD4 expression levels were assessed after differentiation.
- Interleukin-6 (IL-6) production was measured following jacalin stimulation.
- Inhibition studies were performed using anti-CD4 monoclonal antibodies (mAbs), HIV recombinant gp120, and recombinant soluble CD4.
Main Results:
- Jacalin induced a significant increase (10-fold) in IL-6 secretion in CD4+ RA/VD-differentiated U937 cells.
- Jacalin-induced IL-6 production was blocked by anti-CD4 agents and soluble CD4.
- CD4-negative U937 cells differentiated with PMA did not produce IL-6 in response to jacalin, but responded to lipopolysaccharide (LPS).
Conclusions:
- Jacalin induces IL-6 production in CD4+ monocyte/macrophage lineage cells via a CD4-dependent pathway.
- The CD4 molecule plays a crucial role in mediating jacalin's effects on these cells.
- These findings highlight a novel interaction between jacalin, CD4, and cytokine production in macrophages.
Abstract:
The lectin jacalin is mitogenic for CD4 expressing T lymphocytes, interacts with the CD4 molecule, and inhibits HIV infection of CD4+ cells. In the present study the effect of jacalin was tested on cells from the monocyte/macrophage lineage that also express the CD4 molecule. We used CD4+ promyelomonocytic U937 cells differentiated towards the monocytic/macrophage lineage with either a mixture of two physiological agents, retinoic acid (RA) and 1 alpha,25-dihydroxyvitamin D3 (VD), or the exogenous drug phorbol myristate acetate (PMA). The cells resulting from these treatments differed in term of CD4 expression. We focused our attention on interleukin-6 (IL-6) production, which implies an activation of the cells differentiated along both pathways. In CD4+ RA/VD-treated cells, jacalin induced a 10-fold higher IL-6 secretion than did lipopolysaccharide (LPS). This jacalin-induced IL-6 production was inhibited by agents interacting with CD4 (anti-CD4 mAbs and HIV recombinant gp120) or by recombinant soluble CD4. In contrast, the CD4- PMA-differentiated U937 cells did not secrete any IL-6 upon jacalin treatment, while they demonstrated a response to LPS similar to that of the RA/VD-differentiated cells. Together with the fact that jacalin interacts with CD4, these results provide evidence of the involvement of a CD4 dependent pathway in IL-6 production.
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