FIGURE 3 A schematic representation of the proposed mechanisms of action of intravenous immunoglobulin in rheumatic diseases
From the following article:
Monoclonal antibody and intravenous immunoglobulin therapy for rheumatic diseases: rationale and mechanisms of action
Jagadeesh Bayry, Sébastien Lacroix-Desmazes, Michel D Kazatchkine and Srini V Kaveri
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Figure 3. A schematic representation of the proposed mechanisms of action of intravenous immunoglobulin in rheumatic diseases
The mechanisms that underlie the beneficial effects of IVIg involve its direct interaction with various cellular and soluble components of the immune system. IVIg stimulates the expression of Fc
RIIB on a subset of macrophages while blocking the expression of FcRIIA (A). IVIg also modulates cytokine secretion, blocks the expression of Fc receptors and inhibits the activation of macrophages (A) and dendritic cells (B). In addition to inhibition of the activation and production of proinflammatory cytokines by T cells (C), IVIg downregulates DC-mediated T-cell proliferation. At the B-cell level (D), IVIg modulates antibody synthesis and the B-cell repertoire, inhibits B-cell proliferation and induces B-cell-apoptosis. In endothelial cells (E) IVIg blocks the expression of proinflammatory cytokines, chemokines and adhesion molecules. Several other mechanisms of action of IVIg exist: interference with complement activation (F); neutralization of superantigens (G), pathogenic autoantibodies (H) and cytokines (I); sequestration of self antigens (J); induction of ADCC (K) and shifting the balance between T-helper cell subsets (L). The area encompassed by endothelial cells represents the vascular lumen. Adhesion molecules on endothelial cells are depicted. IVIg is depicted in the form of antibody structures with different colors to highlight the fact that it is a polyclonal IgG obtained from pooled plasma from a large number of healthy blood donors. Soluble factors such as complement proteins and cytokines are indicated by colored circles. Abbreviations: ADCC, antibody-dependent cell-mediated cytotoxicity; B, B cell; DC, dendritic cell; EC, endothelial cell; FcR, Fc receptors; NK, natural killer cell; T, T cell.