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Updated: May 15, 2026

In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
Published on: October 15, 2013
IVIg prevents the in vitro activation of T cells by neutralizing the T cell activators
1Department of Research and Development, Héma-Québec, Québec, Canada. lauriane.padet@hema-quebec.qc.ca
Clinical observations in patients treated with IVIg revealed significant modulations in T cell populations and functions. However, it is unclear whether IVIg acts directly on activated T cells to suppress their functions. To clarify the exact mechanism of IVIg action, we studied its effect on T cells activated using anti-CD3/CD28 microbeads to mimic stimulatory signals provided by accessory cells. We report here that IVIg reduces T cell proliferation and cytokine secretion by interfering with the ability of anti-CD3/CD28 microbeads to deliver activating signals to T cells. We further show that the interference occurs between IVIg and anti-CD3/CD28 microbeads and does not involve T cells. In conclusion, our work suggests that T cells are not a direct target of IVIg and that the modulation of T cell populations and functions observed in treated patients is the indirect consequence of a direct effect of IVIg on accessory cells.
Clinical observations in patients treated with IVIg revealed significant modulations in T cell populations and functions. However, it is unclear whether IVIg acts directly on activated T cells to suppress their functions. To clarify the exact mechanism of IVIg action, we studied its effect on T cells activated using anti-CD3/CD28 microbeads to mimic stimulatory signals provided by accessory cells. We report here that IVIg reduces T cell proliferation and cytokine secretion by interfering with the ability of anti-CD3/CD28 microbeads to deliver activating signals to T cells. We further show that the interference occurs between IVIg and anti-CD3/CD28 microbeads and does not involve T cells. In conclusion, our work suggests that T cells are not a direct target of IVIg and that the modulation of T cell populations and functions observed in treated patients is the indirect consequence of a direct effect of IVIg on accessory cells.
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