Inhibition of CD300f function on dendritic cells promotes tumor destruction: Licensing and Research Collaboration Opportunity

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. 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.

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 evaluation under a research collaboration. 

Potential Commercial Applications: 

  • Cancer immunotherapy

Competitive Advantages: 

  • A novel approach

Development Stage: 

  • Pre-Clinical

  • Proof-of-concept studies in mouse models  

Publications:  Tian, L. et al., Enhanced efferocytosis by dendritic cells underlies memory T-cell expansion and susceptibility to autoimmune disease in CD300f-deficient mice. Cell Death and Differ (2016) 23, 1086–1096. 

Intellectual Property:  US Patent Application No. 62/408,596 filed on 10/14/2016;  PCT/US2017/056192 filed on 10/11/2017.

Licensing Contact:  Chris Kornak, 240-627-3705, Chris.Kornak@nih.gov


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NIAID Technology Transfer and Intellectual Property Office

NIAID’s technology transfer office, TTIPO, is a one-stop resource for organizations interested in partnering with NIAID to access, develop, and manage the translation of research discoveries into medically beneficial products. TTIPO seeks to expand NIAID’s innovation pipeline with existing and new partners in areas such as newly emerging and re-emerging infectious diseases (e.g., dengue, Zika, Ebola, influenza, methicillin-resistant Staphylococcus aureus and HIV/AIDS), biodefense (e.g., smallpox and anthrax), and immune-mediated diseases (e.g., asthma and allergy).

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