Abstract

Abstract Intravenous immunoglobulin (IVIg) is a therapeutic preparation of human IgG isolated from thousands of plasma and is currently used for the treatment of an increasing number of immune disorders. A decreased T cell activation was reported in some patients treated with IVIg. To understand the mechanisms responsible for this anti-inflammatory effect, several groups of investigators have performed in vitro assays in which PBMC were activated with immobilized anti-CD3. The main conclusion derived from these works is that IVIg inhibited the functions of activated T cell. However, direct effect of IVIg on activated T cells has been questioned recently. In the present study, we re-examined the mechanisms by which IVIg interferes with the functions of T cells activated with immobilized anti-CD3. First, the level of T cell activation after anti-CD3 stimulation of PBMC, purified T cells or PBMC depleted from monocytes was measured. Our results showed that in the absence of monocytes, T cells did not proliferate in response to anti-CD3 stimulation, suggesting that monocytes are essential to lead to full T cell activation. Second, we evaluated the effect of IVIg on T cell activation after anti-CD3 stimulation of PBMC. Our results showed that T cells were not activated in the presence of IVIg suggesting that not only T cells but also monocytes could be the target of IVIg. Work is underway to better define the role of monocytes in the effects of IVIg on T cell activation.

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