Anti-CD79 Antibody Offers Novel Approach to Therapy in Autoimmune Disease, Transplantation and Lymphoma
Tech ID: 98-04
Summary
Signal transduction by antigen receptors (BCR) is centrally important in many autoimmune diseases, as well as transplant rejection and neoplastic B lymphocyte growth. National Jewish Health researchers discovered that in certain circumstances, subunits of the B cell antigen receptor (BCR) become dissociated rendering the receptor incompetent to transduce activating signals. Based on these observations they produced antibodies against the BCR transducers, CD79a and b, and found that they "desensitize" the BCR and suppress the immune response, autoimmunity, and growth of non-Hodgkins B lymphoma. These anti-CD79 mAbs show therapeutic potential to mediate reversible inhibition of BCR signaling and B cell function. This technology exploits the unique qualities of the BCR to reversibly suppress it for therapeutic use in autoimmunity, cancer and transplantation.
Potential Applications
o Treatment of autoimmune conditions such as rheumatoid arthritis or lupus, lymphatic cancers, allergic diseases
o Prevention of tissue rejection
Advantages of Invention - Method does not deplete B cells as found in current treatments and therefore should be more benign. Should also preserve B cell function in T cell tolerance. It may block the production of autoantibodies by plasmablasts and plasma cells, an effect that current mAb therapy and inhibitors of the BLys family lack.
State of Development
· Receptor desensitization and subsequent prevention of BCR signaling has been demonstrated in vitro and in vivo.
· A monoclonal Ab to CD79 causes B cell receptor dissociation and cell depletion in vivo. F(ab')2 fragments suppress B cell responses without cell depletion.
· In a mouse model of lupus, anti-CD79 decreased autoantibody production, decreased skin pathology, and increased survival.
· Ab to CD79 blocks tumor cell growth in vitro.
Further R&D Required
Testing the antibody in (NZBxNZW)F1 female mice as this models exhibits many features similar to human SLE and developing a humanized mAb to human CD79.
Licensing Potential - Available for licensing
Patent Status - Issued U.S. Patent # 6,503,509; Issued patents in Australia and New Zealand; Patents pending in the US, Europe, Canada, and Japan.
Publication - Vilen et al. 1997. J Immunol . 159(1):231-43; Vilen et al. 1999. Immunity 10:239-248.
Inventors - John Cambier PhD and Barbara J. Vilen, PhD
For Further Information, Contact:
Emmanuel Hilaire
Licensing Associate
Intellectual Property and Technology Commercialization Program
National Jewish Health
1400 Jackson Street, Room M206a
Denver, CO 80206
Voice: (303) 398-1053
Fax: (303) 270-2352
hilairee@njc.org
