Treatment of Viral Infection by Blocking Interleukin-21


Blocking interleukin (IL-21) may be an effective method to treat or prevent various viral infections. In the course of an immune response to a virus, IL-21, produced primarily by CD4+ T cells, can inhibit or stimulate (regulate), immune cell function (B cells, T cells, natural killer cells, dendritic cells). IL-21 regulation may be either protective or pathological; autoimmune disease pathology has been associated with IL-21 promoted inflammation (in: type 1 diabetes, lupus, and multiple sclerosis). This technology describes methods of blocking IL-21 that may reduce damaging inflammatory responses during certain viral infections. Specifically, the absence of IL-21 during respiratory viral infection such as pneumonia virus infection actually prevents some of the pathogenic effects that may be promoted by IL-21. Methods for controlling IL-21 signaling may be used to treat to prevent many pathological effects of pneumonia viruses, and other viral infections.

Potential Commercial Applications: Competitive Advantages:
Prevention and treatment of many pathological effects of viral infections, including pneumonia. New method for treating viral infection pathology.


Development Stage:
  • Early-stage
  • Pre-clinical
  • In vivo data available (animal)


Inventors:

Warren Leonard (NHLBI)  ➽ more inventions...

Rosanne Spolski (NHLBI)  ➽ more inventions...


Intellectual Property:
US Application No. 61/579,801
PCT Application No. PCT/US12/71173
US Application No. 14/367,313

Publications:
Spolski R, et al. PMID 22238461

Collaboration Opportunity:

The NHLBI is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate or commercialize treatment of viral infection by blocking Interleukin-21 (E-017-2012). For collaboration opportunities, please contact Vincent Kolesnitchenko, Ph.D. at kolesniv@nhlbi.nih.gov.


Licensing Contact:
Admin. Licensing Specialist (ALS),
Email:
Phone:

OTT Reference No: E-017-2012-0
Updated: Jun 6, 2012