Intravenous immunoglobulin (IVIG) administration has been beneficially used in the treatment of several autoimmune disorders including myasthenia gravis (MG), although its mechanism of action is still not clear. To study the optimal conditions of IVIG treatment and delineate its mechanism of action we established a suitable model in rat experimental autoimmune MG (EAMG). We show that IVIG has a suppressive effect on the clinical symptoms of ongoing EAMG that is associated with decreased AChR-specific cellular and humoral immune reactivity. Costimulatory factors and cytokine profile analyses suggest that IVIG immunomodulation in EAMG involves suppression of B and Th1-type T cell responses with no generation of T-regulatory cells. Our data contribute to the understanding of the immunological mechanisms underlying IVIG treatment in MG and in other autoimmune disorders.
Bibliographical noteFunding Information:
We thank Prof. Orgad Laub and Dr. Roberto Meidler from Omrix, Nes-Ziona for the preparations of IVIG and for fruitful discussions. This research was supported by grants from The Muscular Dystrophy Association of America (MDA), The Association Francaise Contre les Myopathies (AFM), The European Commission (EC, No QLG1-CT-2001-10918 and QLRT-2001-00225) and The Wood–Byer Foundation.
- Experimental autoimmune myasthenia gravis (EAMG)
- Intravenous immunoglobulins (IVIG)
- Myasthenia gravis (MG)