JAK-STAT Signaling Pathway
Canonical source: KEGG hsa04630
Pathway Overview
The JAK-STAT pathway transduces signals from cytokines (e.g., IL-6, interferons, IL-23) and growth factors to the nucleus, regulating immune responses, cell proliferation, and hematopoiesis. JAKs phosphorylate STATs; STAT dimers translocate and drive transcription. Dysregulation contributes to autoimmune disease (e.g., psoriasis, IBD) and cancer. Environmental triggers include infections and inflammatory stimuli. Key genes include JAK2, STAT3, and cytokine receptors; therapeutics target JAK-STAT in psoriasis and rheumatoid arthritis.
Environmental Triggers
| Exposure | Trigger type |
|---|---|
| psychosocial-stress | Chronic stress can modulate inflammatory cytokines |
| diet-quality | Dietary components may affect systemic inflammation |
Genetic Modulation Points
No genetic modulation points recorded.
Tissue Specificity
No tissue specificity data recorded.
Disease Relevance
Linked diseases
- psoriasis— IL-23/Th17 axis; therapeutic target
- rheumatoid-arthritis— Cytokine-driven inflammation
- inflammatory-bowel-disease— IL-23/Th17; JAK inhibitors in development
Linked exposures
- psychosocial-stress— Stress-immune axis
Pathway Diagram
Pathway diagram placeholder. A visual representation of this pathway will be integrated when available.
Evidence Nodes
Evidence for this pathway is derived from:
- 2 environmental trigger(s)
- 3 linked disease(s)
- 1 linked exposure(s)
References
- 1.O'Shea JJ, et al. (2015). JAK-STAT signaling in immune regulation. Immunity. doi:10.1016/j.immuni.2015.02.010
- 2.Schwartz DM, et al. (2017). Targeting the JAK/STAT pathway in autoimmune disease. Nature Reviews Drug Discovery. doi:10.1038/nrd.2017.201