Normal IgG protects against acute graft-versus-host disease by targeting CD4+CD134+ donor alloreactive T cells

Inhibition of maturation and function of dendritic cells by intravenous immunoglobulin

“…This latter effect of IVIg is of potential relevance considering its beneficial effect in autoimmune conditions and graft-versus host disease. 32,39 Insufficient IL-12 production and decreased expression of CD80 by APCs, with concomitant increased secretion of IL-10 that in turn blocks DC maturation and inhibits IL-12 production during antigen presentation, have been implicated in the induction of anergy and tolerance of T cells. [40][41][42] The fact that IVIg blocks phenotypic and functional maturation was further substantiated by its ability to block autologous and allogeneic MLR.…”

Use of intravenous immunoglobulin in human disease: A review of evidence by members of the Primary Immunodeficiency Committee of the American Academy of Allergy, Asthma and Immunology

“…216 Intact IgG molecules and F(ab) 2 fragments of IgG protect against acute GVHD in a rat model of the disease. 219 Protection was associated with decreased lymphocyte proliferation and decreased nitrous oxide and IFN-g production in vitro in the absence of increased production of IL-10. A recent US multicenter, randomized, double-blind comparison of 3 different doses of IGIV (0.1, 0.25, and 0.5 g/kg), however, showed no differences in the rates of acute or chronic GVHD or infection after unrelated allogeneic bone marrow transplantation.…”

Modulation of the cellular immune system by intravenous immunoglobulin

“…Interestingly, IVIg can directly bind to activated, but not to resting rat T cells, thus indicating FcgR-independent interaction of IVIg with T cells [53]. In addition, IVIg treatment protects against GvHD in rats, which is associated with decreased proliferation of lymphocytes, reduced production of IFNg and enhancement of apoptosis of activated T cells [54]. Reduced proliferative responses of T cells might also explain the beneficial effect in lupus-like syndrome and atherosclerosis in mice [55,56].…”