Use Of Viral Il-6 To Modulate Monocyte Differentiation To Boost Anti-Tumor Immunity
Tech ID: 33317 / UC Case 2022-582-0
Researchers at the University of California, Davis have developed a virally derived homolog to increase the inflammatory response desirable in cancer immunotherapy.
Researchers at the University of California Davis have developed the use of a virally derived homolog of interleukin-6 (vIL-6) to increase the inflammatory response desirable in cancer immunotherapy. The technology promotes dendritic cell differentiation and M1 macrophage differentiation from monocytes, unlike human IL-6, and doesn't trigger anti-inflammatory negative feedback mechanisms. The technology includes the RNA- and viral vector-based delivery of vIL-6-encoding nucleic acids.
Unlike IL-6, vIL-6 does not trigger negative feedback regulation, thus providing a unique benefit when it's used therapeutically as it does not limit its own efficacy by self-downregulation. This new technology aims to enhance cancer therapy by combining the administration of vIL-6 with an anti-cancer therapeutic agent, especially an anti-cancer immunotherapeutic agent.
- Development of new medication and treatments for cancer
- Potential use in research and development in the medical and pharmaceutical industry
- Useful in the field of cancer therapeutics, specifically in immunotherapy
- Potential application in the manufacturing of cell culture mediums
- May be incorporated into various delivery systems such as viral vector-based delivery, liposomal formulations, transdermal patches, etc for treating cancer
- Increases the inflammatory response desirable in cancer
- Promotes dendritic cell differentiation and M1
- Utilizes RNA- and viral vector-based delivery
for effective implementation
- Does not self-downregulate which is an issue
with existing therapies that are limited by negative feedback mechanisms
- Can be applied in various formats such as
protein form or nucleic acid form
- Potential supplement for cell culture to enhance the
recovery and efficacy of dendritic cells