Difference between revisions of "Team:ColumbiaNYC/Brainstorm"
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| + | <h2>T-cell Targeted Nociceptive Sodium Channels</h2> | ||
| + | <p>Nav1.7 is a voltage-gated sodium channel expressed on nociceptive neurons, neurons responsible for transmitting pain signals from the PNS to the CNS. | ||
| + | Nav1.7 is essential for normal pain sensation; if it is not expressed, the patient will not feel pain at all, and if it is overexpressed, the patient will experience chronic pain (20% of the population worldwide). | ||
| + | Nav1.7 is therefore a prime therapeutic target whose blockage by an T-cell antibody would mitigate pain, with the T cell acting as a potential analgesic. | ||
| + | A circuit would be designed so that once the T cell binds to the epitope, a chimeric antigen receptor (CAR) could be engineered to be drug-switchable so that the T cells are controllable, which is not currently the case. | ||
| + | This way, a physician could titrate cell activity and control timing with a drug, which is potentially safer. </p> | ||
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Revision as of 15:04, 7 July 2017
Brainstorming
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T-cell Targeted Nociceptive Sodium Channels
Nav1.7 is a voltage-gated sodium channel expressed on nociceptive neurons, neurons responsible for transmitting pain signals from the PNS to the CNS. Nav1.7 is essential for normal pain sensation; if it is not expressed, the patient will not feel pain at all, and if it is overexpressed, the patient will experience chronic pain (20% of the population worldwide). Nav1.7 is therefore a prime therapeutic target whose blockage by an T-cell antibody would mitigate pain, with the T cell acting as a potential analgesic. A circuit would be designed so that once the T cell binds to the epitope, a chimeric antigen receptor (CAR) could be engineered to be drug-switchable so that the T cells are controllable, which is not currently the case. This way, a physician could titrate cell activity and control timing with a drug, which is potentially safer.
