What is the mechanism of action of RhIG in the treatment of ITP?
How RhIG works is unclear but blockade of Fc receptors within the reticuloendothelial system (RES) is believed to be the primary mechanism of action. Possible mechanisms include:
- Infused RhIG competitively inhibits FcR-mediated binding of platelets by macrophages within the RES. Specifically, RhIG binds to autologous Rh positive red cells leading to sequestration in the spleen and blocking of RES, allowing prolonged survival of IgG-coated platelets.
- Other mechanisms include diminished macrophage FcR number and binding affinity, altered platelet binding, suppression of T-cell and B-cell function, changes in cytokine production.
- RhIG may cause immunomodulation but data to support this are limited.