Neutralization of mitogenic lectins by intravenous immunoglobulin (IVIg) prevents T cell activation: does IVIg really have a direct effect on T cells?

Intravenous Immunoglobulin as a Potential Therapy for Refractory Urticaria - A Review

“…Correia et al and Darras et al also reported on remission of severe solar urticaria in single patients following high dose IVIG infusion [51,52]. While the poor response seen in the one report by Llamas-Velasco et al, may have been due to differences in product or dosage protocol, it is also quite possible that solar urticaria is a heterogeneous disease, with Alters cellular recruitment [37,43] Limits complement activation and dampens complement-mediated vascular and tissue injury [37] Inhibits inflammatory cytokines and induces inhibitory cytokines By altering Th1/2 or Th17 maturation as well as modulating glucocorticoid receptors or Fcgamma receptors on T cells and inflammatory cells [34,42,44,45] or by inhibiting T cell activation [5,37] Decreased adhesion to endothelial cells [43] Adaptive Immunity…”

“…Antigen presentation is affected by decreased expression of costimulatory molecules such as CD40, CD80/86 or HLA molecules. T regulatory cells may be induced by IVIG by upregulation of CD25+/CD4+/FOXP3+ or via complex cytokine pathways [5,37,42,44,45]. Anthony et al have recently reported that some of the observed anti-inflammatory effects of IVIG are mediated by a minor population of IgG crystallizable fragments that possess glycans and sialic acids that bind to DC-SIGN (dendritic cell specific ICAM-3 grabbing non-integrin) [42].…”

“…Decreased activation [5] due to APC or B cell functional defects Increased regulation by T regulatory cells [5,34,37,41] Induced by upregulation of CD25+/CD4+/FOXP3+ or via complex cytokine pathways [5,37,42,44,45] Decreases activation by decreasing TLR-9 receptor expression Induces B cell apoptosis via CD22 or Fc RIIb Directly inhibits B cell growth factors (BAFF, APRIL) [37,41,46] some forms being responsive to IVIG and other forms being resistant [23].…”

“…When accompanied by fever, elevated sedimentation rate, arthralgias and multisystem involvement, urticarial vasculitis should also be suspected [1,3]. In some cases, urticaria may be a manifestation of systemic anaphylaxis, which can be fatal [4,5]. In such situations, common causes include reactions to medication, food allergen, injected venoms or hormones (such as progesterone).…”

Polyclonal immunoglobulin G for autoimmune demyelinating nervous system disorders

“…It may skew peripheral blood T cell subsets in multiple beneficial ways, including suppression of pro-inflammatory Th17 cells [25][26][27], promotion of protective CD4/CD25/FoxP3-positive T regulatory cells [28][29][30][31][32], induction of a protective Th1/Th2 shift [33][34][35], and inhibition of CD8-positive cytotoxic T cell activation and expansion [36,37]. Importantly, polyclonal IgG may inhibit T cell interactions with antigen-presenting cells by binding to T cell surface receptors, including the T cell receptor b-chain, HLA molecules, and costimulatory molecules such as CD28 [38][39][40][41]. In addition, it was demonstrated that polyclonal IgG inhibits the in vitro proliferation of human T cell lines reactive against myelin basic protein (MBP) [42].…”