Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthful human plasma through Cohn fractionation. The purification technique consists of cold alcohol fractionation, polyethylene glycol precipitation, and ion change chromatography. IVIg includes the equal distribution of IgG antibody subclasses as is discovered in the preferred human populace. IgG subclasses are fully represented in the following proportions: 70.three% IgG1, 24.7% IgG2, three.1% IgG3, and 1.nine% IgG4. IVIg is used inside the treatment of immunodeficiencies, as well as autoimmune and inflammatory issues.
Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens.
IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-BarrÃ© syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskottâ€“Aldrich syndrome and inflammatory skin diseases.
IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage â€œtaggingâ€ or neutralization (via binding) of pathogen toxins. Intact IVIg and F(abâ€²)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components.