Intravenous immunoglobulin suppresses experimental myasthenia gravis: immunological mechanisms.
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.
Zhu
Kai-Yun
KY
Department of Immunology, Weizmann Institute of Science, Rehovot 76100, Israel.
Feferman
Tali
T
Maiti
Prasanta K
PK
Souroujon
Miriam C
MC
Fuchs
Sara
S
D000818:Animals; D005260:Female; D007074:Immunoglobulin G / Q000097:blood / Q000145:classification; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use*; D016753:Interleukin-10 / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D008213:Lymphocyte Activation; D020720:Myasthenia Gravis, Autoimmune, Experimental / Q000276:immunology / Q000517:prevention & control*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011917:Rats, Inbred Lew; D011950:Receptors, Cholinergic / Q000276:immunology; D015375:Receptors, Interleukin-2 / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000235:genetics
D007074:Immunoglobulin G; D016756:Immunoglobulins, Intravenous; D012333:RNA, Messenger; D011950:Receptors, Cholinergic; D015375:Receptors, Interleukin-2; D016212:Transforming Growth Factor beta; D016753:Interleukin-10; D015847:Interleukin-4