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The Janus kinase–signal transducer and activator of transcription (JAK–STAT) pathway is utilized by a range of cytokines (interferons, IL-2 and IL-6 amongst others) that control survival, proliferation and differentiation responses in diverse cell types. The realisation that unregulated activation of this pathway is a key driver of not only chronic inflammatory diseases such as rheumatoid arthritis, colitis and psoriasis, but also many cancers has identified its components as targets for therapeutic intervention by small molecule inhibitors and biologicals. In this article, we will discuss how an increased understanding of JAK-STAT pathway architecture, the basis for its dysfunction in pathological states, and its regulation by other intracellular signaling pathways are illuminating multiple strategies to manipulate this pathway in several disease arenas.

Cross-Regulation of JAK-STAT Signaling: Implications for Approaches to Combat Chronic Inflammatory Diseases and Cancers