Inhibition of CD300f Function on Dendritic Cells Promotes Tumor Destruction

Cancer immunotherapy aims to enhance the ability of a patient’s own immune response to destroy tumors. The magnitude of the immune response is determined by the balance between immune activating signals and negative inhibitory signals. Checkpoint receptors are negative regulators that normally deliver inhibitory signals which limit immune activation. Blockade of immune checkpoints represents an effective strategy to enhance the immune response against cancer cells.

NIAID researchers have discovered that blocking CD300f function in dendritic cells markedly enhances their ability to phagocytose and process apoptotic tumor cells, leading to substantial inhibition of tumor growth. In this light, CD300f may be viewed as a dendritic cell checkpoint receptor analogous to T cell checkpoint receptors like PD-1 and CTLA-4. As a result, inhibiting CD300f function on dendritic cells could be a promising anti-cancer therapy, especially in the settings where blocking of T cell checkpoint receptors has been ineffective.

This technology is available for licensing for commercial development in accordance with 35 U.S.C. § 209 and 37 CFR Part 404, as well as for further development and

Potential Commercial Applications:		Competitive Advantages:
Cancer immunotherapy		A novel approach

Inventors:

John Coligan (NIAID)  ➽ more inventions...

Konrad Krzewski (NIAID)  ➽ more inventions...

Linjie Tian (NIAID)  ➽ more inventions...

Ha Na Lee (NIAID)  ➽ more inventions...


Intellectual Property:
US Application No. 62/408,596
PCT Application No. PCT/US2017/056192

Publications:
Tian L, et al. PMID: 26768664

Collaboration Opportunity:
For collaboration opportunities, please contact Chris Kornak at chris.kornak@nih.gov or 1-240-627-3705.


Licensing Contact:
Christopher Kornak, J.D.
Email: chris.kornak@nih.gov
Phone: 240-627-3705

OTT Reference No: E-257-2016-0
Updated: Jul 23, 2018