Insulin-Like Growth Factor Binding Proteins in Autoimmune Diseases

Figures

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  Figure 1. Common structure and biological function of IGFBPs. (A) The N-terminal region (blue) and the C-terminal region (yellow) are connected by a linker region (green). Both N-domain and C-domain contains a binding site for IGFs (orange). (B) The proteolysis of IGFBPs by various proteases (pink) occurs in the linker region or other post-translational modifications, may result in IGFs release. (C) Once released from IGFBPs, IGFs bind to IGF receptors (purple) to exert their physiological effects.

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  Figure 2. Scheme of possible mechanisms by which autoimmune diseases are mediated by IGF-IGFBP signaling pathways. Immune cell proliferation may be partly dictated by IGF-IGFBP pathway. The inhibition of regulatory immune cells or the control of gene transcription of proinflammatory cytokines may be mediated by IGF-independent pathways such as IGFBP3, TGF-β, and GPCR etc. STAT: Signal transducer and activator of transcription including STAT1, STAT2, STAT3, and STAT4.