Cytokine storm–related pathways

Cytokine storm–related pathways encompass the complex signaling networks, including the JAK/STAT, NF-κB, and MAPK cascades, that drive the uncontrolled and excessive release of pro-inflammatory cytokines (PMC, 2021) [2, 4]. This biological phenomenon, often termed a cytokine storm or cytokine release syndrome (CRS), results from a dysregulated immune response where a self-amplifying feedback loop leads to systemic hyperinflammation (CAS, 2022) [1, 5]. These pathways are typically triggered by severe infections (such as SARS-CoV-2 or influenza), certain cancers, or therapeutic interventions like CAR T-cell therapy (MDPI, 2023) [12]. The resulting surge in mediators such as IL-6, TNF-α, and IL-1β can cause widespread tissue damage, vascular leakage, and multi-organ failure (PMC, 2021) [4]. Therapeutic strategies involve the use of monoclonal antibodies to block cytokine receptors or small molecules to inhibit intracellular signaling kinases, thereby dampening the inflammatory response (Atlantis Press, 2021) [9]. However, modulating these pathways carries significant risks, including profound immunosuppression and an increased susceptibility to secondary bacterial or fungal infections (MDPI, 2023) [12].

Other names

Cytokine release syndrome pathwaysHypercytokinemia pathwaysInflammatory storm pathwaysCRS-related pathways

Inhibition of cytokine-receptor binding, suppression of intracellular signaling cascades (e.g., JAK/STAT), and modulation of pro-inflammatory gene transcription.