This is supported by significantly increased numbers of NKT cells after alcohol intake. NKT cells can inhibit diabetes onset by impairing the development of pathogenic T cells specific for pancreatic beta cells. Additional effects that may act in concert cannot be excluded;U0126 alcohol impairs cytokine-driven differentiation and function of myeloid and plasmacytoid dendritic cells in vitro. NKT cells are potent regulators that can inhibit development of T1D by impairing the differentiation of anti-islet T cells into Th1 effector cells, and for doing this cell contact seems to be crucial. However still for raising the NKT cells the CD1d presentation is decisive. Intravenous immunoglobulin G is a therapeutic immunoglobulin G preparation derived from pooled plasma of at least 1000 healthy blood donors. It was initially developed as a replacement agent for treating primary and secondary antibody deficiencies. However,VE-822 since nearly three decades immune modulating therapy of acute and chronic autoimmune diseases became a second major clinical indication for IVIg therapy. Many patients with acute and chronic autoimmune diseases benefit from IVIg treatment, although its use is not in all cases effective. Fromclinical studies it is known that IVIg therapy is effective in the treatment of antibodydependent thrombocytopenia such as idiopathic thrombocytopenic purpura. The main protective effect of IVIg in ITP seems to be the inhibition of the Fcc receptor mediated phagocytosis. By injecting a high dose of IVIg Fcc receptor-bearing phagocytic cells in the spleen are blocked and thereby prevent the destruction of antibody opsonized platelets. F 2 fragments of IVIg are not able to inhibit platelet clearance in a murine model of thrombocytopenia. Besides the Fcc receptor inhibition, another reason for the high dose of IVIg required for therapeutic efficacy could be that only a fraction of IVIg is causing the desired effects. Identification of this fraction of IVIg would possibly allow the development of a more effective IVIg preparation with a changed composition designed for treating patients with autoimmune diseases. A recent study indicated that the Fc-sialylated IgG fraction is the active immunomodulating entity in IVIg.