Deucravacitinib, a selective TYK2 inhibitor, offers precision immunomodulation by bridging cytokine storm and chronic inflammation.

Inflammation is a dynamic continuum, transitioning from acute cytokine storm to persistent chronic inflammation through unresolved immune dysregulation. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is central to this process, with tyrosine kinase 2 (TYK2) acting as a critical regulatory node. TYK2 integrates signals from type I interferons, interleukin-12 (IL-12), and interleukin-23 (IL-23), driving inflammatory responses. Current treatments often lack specificity, leading to broad immunosuppression; thus, targeting specific nodes like TYK2 offers a pathway for precision immunomodulation.

This comprehensive review synthesizes molecular events linking acute cytokine storm to chronic inflammation, focusing on the JAK-STAT pathway and TYK2's pivotal role. It delineates how immune cell activation, cytokine network architecture, and intracellular signaling cross-talk evolve into persistent immune dysregulation. The review specifically evaluates deucravacitinib's mechanism as a selective allosteric TYK2 inhibitor and highlights its therapeutic implications, drawing from published clinical trial data on its efficacy and safety profile in psoriasis and other immune-mediated disorders.

The review establishes TYK2 as a central mediator, integrating signals from type I interferons, IL-12, and IL-23 to sustain inflammatory signaling across disease stages. It details how TYK2 bridges innate and adaptive immune responses, contributing to immune cell reprogramming, epigenetic modifications, and loss of immune tolerance that drive the transition from acute hyperinflammation to chronic disease. Deucravacitinib, a selective allosteric TYK2 inhibitor, modulates TYK2 signaling with high specificity, offering a targeted approach. Clinical trial data consistently demonstrate its efficacy and favorable safety profile in psoriasis and other immune-mediated disorders.

Deucravacitinib's targeted action on TYK2 positions it as a promising strategy for precision immunomodulation, interrupting the inflammatory progression continuum.