Novel Leukocyte Receptor and Allograft Rejection

Award Information
Agency:
Department of Health and Human Services
Branch
n/a
Amount:
$75,000.00
Award Year:
1994
Program:
SBIR
Phase:
Phase I
Contract:
1 R43 AI36755-1,
Agency Tracking Number:
24799
Solicitation Year:
n/a
Solicitation Topic Code:
n/a
Solicitation Number:
n/a
Small Business Information
Activated Cell Therapy, Inc.
291 N Bernardo Avenue, Mountain View, CA, 94043
Hubzone Owned:
N
Socially and Economically Disadvantaged:
N
Woman Owned:
N
Duns:
n/a
Principal Investigator:
Curtis Ruegg
(415) 964-6744
Business Contact:
() -
Research Institution:
n/a
Abstract
We will extend recent observations regarding the discovery and characterization of alloreaction-a-ssociated antigen (ARAg), a novel member of the immunoglobulin gene superfamily selectively expressedon leukocyte subsets. ARAg surface expression is increased on T lymphocytes in response to allogeneic,but not by mitogenic, stimuli and anti-ARAg monoclonal antibody (mAb) P1C5 specifically blocks thisalloactivation response in vitro. There are two aims of this proposal: 1) to provide evidence for theexistence of a putative ARAg counter-receptor (ARAg-CR) expressed which presumably interacts withARAg in transduction of important activation signals, and 2) to isolate a cDNA clone encoding the murinehomologue of ARAg. Soluble recombinant ARAg proteins will be engineered and used in flow cytometryassays to examine phenotypic expression of the putative ARAg-CR on relevant cell types. Evidence forthe existence of a putative ARAg-CR will provide an additional target for potential pharmacologicintervention. Molecular cloning of the murine ARAg homologue is essential for development of an animalmodel in which to evaluate candidate ARAg-based therapeutics in vivo. The long-term objective of thisproject is to develop ARAg-related reagents for their potential therapeutic value in allograft rejection andGVHD as well as autoimmune disease and reperfusion injury.

* information listed above is at the time of submission.

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