This technology describes a method for immunomodulation via alteration of the length of 3’ Untranslated Regions (3’ UTRs) to control inflammation, which may be relevant in developing immunotherapies or neuroinflammatory therapies.
Loss of RNA homeostasis is known to contribute to various neurodegenerative and neuroinflammatory diseases, but the molecular mechanisms promoting these inflammatory pathways are unclear. Viral double-stranded RNAs (dsRNAs) are known to promote innate immune responses, but the mechanisms underlying these processes and how they may be targeted therapeutically have not been extensively explored. Studying the pathways through which dsRNAs can trigger neuroinflammation can identify therapeutic targets for neuroinflammatory diseases, as well as cancer immunotherapies. Assessing the protective versus pathogenic role of dsRNAs and their association with 3’UTR lengths can be useful to better understand neuron-specific toxic inflammation.
This technology identifies molecular mechanisms that can alter double-stranded (dsRNA) levels in different cell types to target toxic inflammation and the loss of RNA homeostasis. This technology distinguishes the association between mRNAs with elongated 3’ Untranslated Regions (3’ UTRs) and immunogenic dsRNAs. Fine-tuning 3’ UTR length and specifically inducing 3’ UTR lengthening can be used to promote an immune response, indicating mechanisms to boost or suppress immune responses and inflammation. Immunomodulation via the modification of the length of 3’ UTRs can be used to develop therapies for neurodegenerative and neuroinflammatory diseases as well as cancer immunotherapies.
This technology has been validated with human stem cell lines.
Patent Pending (WO/2024/249458)
IR CU23300
Licensing Contact: Jerry Kokoshka