The "Heater" of "Cold" Tumors-Blocking IL-6.
Weigao PuChenhui MaBofang WangWeidong ZhuHao ChenPublished in: Advanced biology (2024)
The resolution of inflammation is not simply the end of the inflammatory response but rather a complex process that involves various cells, inflammatory factors, and specialized proresolving mediators following the occurrence of inflammation. Once inflammation cannot be cleared by the body, malignant tumors may be induced. Among them, IL-6, as an immunosuppressive factor, activates a variety of signal transduction pathways and induces tumorigenesis. Monitoring IL-6 can be used for the diagnosis, efficacy evaluation and prognosis of tumor patients. In terms of treatment, improving the efficacy of targeted and immunotherapy remains a major challenge. Blocking IL-6 and its mediated signaling pathways can regulate the tumor immune microenvironment and enhance immunotherapy responses by activating immune cells. Even transform "cold" tumors that are difficult to respond to immunotherapy into immunogenic "hot" tumors, acting as a "heater" for "cold" tumors, restarting the tumor immune cycle, and reducing immunotherapy-related toxic reactions and drug resistance. In clinical practice, the combined application of IL-6 inhibition with targeted therapy and immunotherapy may produce synergistic results. Nevertheless, additional clinical trials are imperative to further validate the safety and efficacy of this therapeutic approach.
Keyphrases
- oxidative stress
- inflammatory response
- clinical trial
- signaling pathway
- clinical practice
- induced apoptosis
- end stage renal disease
- stem cells
- chronic kidney disease
- newly diagnosed
- risk assessment
- palliative care
- ejection fraction
- cancer therapy
- endothelial cells
- single molecule
- endoplasmic reticulum stress
- drug induced
- lps induced