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Inhibiting DNA Repair Activity in Rheumatoid Arthritis


Stanford Reference:

10-255


Abstract


A team of Stanford researchers have identified a novel immune-protective approach for treating rheumatoid arthritis (RA) and other disorders of immune system function. By studying the T cells of patients with rheumatoid arthritis, the inventors discovered that the DNA-dependent protein kinase (DNA-PK) enzyme, which in turn activates the JNK pathway, is implicated in accumulated DNA damage and premature T cell aging and apoptosis. Therapies that target these pathways could restore DNA repair mechanisms and rejuvenate the immune system to treat RA and other diseases characterized by chronic immune responses.

Current RA therapeutics, which aim to generally reduce inflammation or activation of immune response, have major side effects of infections and potentially tumor development. This alternative approach, with agents that target apoptotic machinery to rescue T cells from dying, is unlikely to impair the patient’s immune system.

Ongoing Research
The inventors continue to study the upstream and downstream events connected to DNA-PK activity and how it affects T cell function.


Applications


  • Therapeutic - to reduce apoptosis and improve immune system function in rheumatoid arthritis and other diseases characterized by accelerated immune aging

Advantages


  • Improves immune competence - in contrast with current non-specific, inflammation-targeted therapies that compromise immune function and can lead to side effects of infections and potential tumor development
  • Upstream intervention - targeting DNA repair could preserve tissue because it acts upstream of tissue-damaging inflammation

Publications



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Innovators & Portfolio



Date Released

 4/2/2012
 

Licensing Contact


Chu Chang, Licensing Associate
650-723-0652 (Direct)
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Related Keywords


apoptosis    DNA repair   immune cells   protein kinase   protein kinase inhibitors   rheumatoid arthritis   rheumatology   
 

   

  

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