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Glucocorticoid-induced TNFR Family-Related Receptor Ligand (GITRL) Antibodies for Diagnosis and Treatment of Immune System Disor

Posted Nov 15 2012 7:00pm

Description of Invention:
This technology provides novel antibodies and methods for diagnostics and treatment of disorders arising from dysregulation of the immune system using antibodies directed against glucocorticoid-induced tumor necrosis factor receptor family-related receptor ligand (GITRL). Also available are hybridomas producing anti-mouse GITRL monoclonal antibodies (clone 5F1).

Glucocorticoid-induced TNFR family-related receptor (GITR, also known as TNFRSF18) is expressed on the surface of responder T cells (CD4+CD25- or CD8+CD25- T cells). Upon activation of the immune response, GITR is up-regulated and binds to its ligand, GITRL (also known as TNFSF18), which enhances the immune response. The inventors have developed anti-GITRL monoclonal antibodies that block the interaction between GITR and GITRL, and have demonstrated in in vitro experiments that administration of these blocking antibodies can suppress the immune response. These antibodies may be useful for treatment of immune system disorders such as multiple sclerosis, rheumatoid arthritis, and other inflammatory diseases.

  • Development of therapeutic agents for autoimmune diseases, including autoimmune and inflammatory diseases, allergy and transplant rejection.
  • Tool for investigating the role of GITRL in enhancement of the T-cell mediated immune response.

The GITR/GITRL pathway is a novel target for the treatment of autoimmune diseases.

Development Status:
  • In vitro data available
  • In vivo data available (animal)

Ethan M Shevach (NIAID)

Patent Status:
HHS, Reference No. E-229-2003/2
US, , Patent No. 7,618,632, Issued 17 Nov 2009

Relevant Publication:
  1. Stephens GL, et al. [ PMID 15470044 ]

For Licensing Information Please Contact:
Tara Kirby Ph.D.
NIH Office of Technology Transfer
6011 Executive Blvd. Suite 325,
Rockville, MD 20852
United States
Phone: 301-435-4426
Fax: 301-402-0220

Ref No: 2501

Updated: 11/2012

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