IFN gamma, also known as IFNG, is a secreted protein which belongs to the type I I interferon family. IFN gamma is produced predominantly by natural killer and natural killer T cells as part of the innate immune response, and by CD4 and CD8 cytotoxic T lymphocyte effector T cells once antigen-specific immunity develops. IFN gamma has antiviral, immunoregulatory, and anti-tumor properties. IFNG, in addition to having antiviral activity, has important immunoregulatory functions, it is a potent activator of macrophages, and has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of the type I interferons. The IFNG monomer consists of a core of six &alpha,-helices and an extended unfolded sequence in the C-terminal region. IFN gamma is critical for innate and adaptive immunity against viral and intracellular bacterial infections and for tumor control. Aberrant IFN gamma expression is associated with a number of autoinflammatory and autoimmune diseases. The importance of IFN gamma in the immune system stems in part from its ability to inhibit viral replication directly, and most importantly from its immunostimulatory and immunomodulatory effects. IFNG also promotes NK cell activity.
The insulin-like growth factor binding protein (IGFBP) family consists of six structurally related proteins that bind IGF with high affinity. These proteins share conserved cysteine-rich N-and C-terminal regions that participate in IGF binding. IGFBPs regulate the bioavailability of IGFs and modulate their biological activities, both positively and negatively. Some IGFBPs also have intrinsic bioactivity that is IGF-independent. Post-transitional modifications of the IGFBPs, including glycosylation, phosphorylation and proteolysis, influence IGF binding affinities and tissue localization, affecting both the IGF-dependent and independent functions.
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