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HHS Recovery Act Recipient Reporting Readiness Tool

Step 4. Review and Copy the Grant Awards Data

TAGGS provides some – but not all – of the data needed for the Recipient Report. Recipients are responsible for directly collecting and reporting all required data to FederalReporting.gov. Data that HHS does not currently collect are highlighted in yellow. Do not copy this highlighted information. Please enter the appropriate data for your organization in these required fields. For assistance with entering these data please contact FederalReporting.gov.

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Award Detail for: EPIGENETIC CONTROL OF T CELL AUTOIMMUNITY
UNIVERSITY OF MINNESOTA, OFFICE OF STUDENT FINANCE AID
DUNS Number: 555917996
106 PLEASANT SE, 210 FRASER HL
MINNEAPOLIS, MN 55455
Recipient Report: Grant or Loan
Prime Recipient

Reporting Information
Award Type Award Number Final Report
Grant 1R01AI080764-01A1 Recipient responsible for this data

Award Recipient Information
Recipient DUNS Number Recipient Account Number Recipient Congressional District
555917996 Recipient responsible for this data 5

Award Information
Funding Agency Code Awarding Agency Code Award Date
7529 7529 08-11-2009
Amount of Award Sub Account Number for Program Source (TAS)  
$ 377,500 Recipient responsible for this data
Program Source (TAS)* CFDA Number 
750900 93.701
Total Number of Sub Awards to Individuals Total Amount of Sub Awards to Individuals
Recipient responsible for this data Recipient responsible for this data
Total Number of Payments to Vendors less than $25,000/award Total Amount of Payments to Vendors less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Total Number of Sub Awards less than $25,000/award Total Amount of Sub Awards less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Award Description
Effective control of systemic autoimmune diseases such as rheumatoid arthritis (RA) currently relies on the use of intense generalized immunosuppression, thus increasing the risk of infection and malignancy. A better theoretical approach to the treatment of autoimmune disease is the induction of an antigen-specific tolerance that targets only the dangerous self-reactive T and B cells. The design of such effective therapies with the potential to cure autoimmune disease, however, is hampered by our inability to visualize and study those self antigen-specific polyclonal lymphocytes within the intact immune system. Furthermore, we lack sufficient knowledge regarding the induction of clonal anergy in lymphocytes that are already responding to self antigens within the diseased individual. Finally, our typical candidate approach to the identification of new therapeutic targets is an inherently slow process that can be adversely influenced by preconceived notions about the molecular mechanisms that are important to the induction of anergy. We now propose a series of pre-clinical studies that will make use of emerging antigen/class II tetramer technologies to track polyclonal CD4+ T cells that break immune tolerance and cause autoimmunity. Specific Aim 1 will investigate the individual roles of NT5'E and Foxp3 in the development and maintenance of clonal anergy following initial self antigen encounter by polyclonal CD4+ T cells in the peripheral immune system. Ecto-5'-nucleotidase (NT5'E), a novel candidate anergy factor discovered using a genome-wide screen for chromatin modifications in association with changes in gene expression, will be evaluated for its role in the control of clonal anergy development and maintenance of antigen unresponsiveness. Specific Aim 2 will establish the role of clonal anergy in the epigenetic changes that protect against the development of CD4+ T cell-mediated arthritis. Experiments under this aim will model RA using an adoptive transfer of KRN TCR-transgenic T cells reactive to the natural autoantigen glucose-6-phosphate isomerase (GPI), and investigate in the setting of systemic inflammation or lymphopenia the roles of NT5'E and Foxp3+CD4+ T regulatory cells in the epigenetic control of clonal anergy induction. In addition to increasing our fundamental knowledge about the regulation of anergy induction by NT5'E and immunoregulation in vivo, the results obtained with the class II tetramers will also serve as a paradigm for the development of biomarkers for use in human trials designed to target autoreactive CD4+ T cells for clonal anergy induction. Furthermore, our ongoing investigation of the epigenetic control of gene expression during CD4+ T cell responses to self antigen offers the opportunity to identify additional novel therapeutic targets. PUBLIC HEALTH RELEVANCE: The development of a cure for diseases such as rheumatoid arthritis will require the design of therapies that can effectively restore immune self tolerance in T cells. To develop such therapies, we need to create tools that can monitor the state of tolerance in offending T cells during human trials. Furthermore, we need to discover additional molecular targets for therapeutic intervention that will promote tolerance induction in autoreactive T cells. This project will develop the appropriate tools to monitor the behavior of autoreactive T cells in several mouse models of autoimmunity, will test one potential therapeutic target (NT5'E) for its role in tolerance induction, and will take advantage of new gene array technology to discover additional therapeutic targets.

Project Information
Project Name or
Project/Program Title
Project Status Total Federal Amount ARRA Funds
Received/Invoiced
EPIGENETIC CONTROL OF T CELL AUTOIMMUNITY Recipient responsible for this data Recipient responsible for this data
Number of Jobs Description of Jobs Created
Recipient responsible for this data Recipient responsible for this data
Quarterly Activities/Project Description
Recipient responsible for this data
 
Activity Code (NAICS or NTEE-NPC)
1Recipient responsible for this data2Recipient responsible for this data
3Recipient responsible for this data4Recipient responsible for this data
5Recipient responsible for this data6Recipient responsible for this data
7Recipient responsible for this data8Recipient responsible for this data
9Recipient responsible for this data10Recipient responsible for this data
Total Federal Amount of ARRA
Expenditure
Total Federal ARRA
Infrastructure Expenditure
Infrastructure Contact Name
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Email Infrastructure Contact Phone Infrastructure Contact Phone Ext.
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Street Address 1 Infrastructure Contact Street Address 2 Infrastructure Contact Street Address 3
106 PLEASANT SE, 210 FRASER HL Not Available Recipient responsible for this data
Infrastructure City Infrastructure State Infrastructure ZIP Code+4
MINNEAPOLIS MN 55455
Infrastructure Purpose and Rationale
Recipient responsible for this data

Primary Place of Performance
Street Address 1 Street Address 2 City
3-280 MBB Recipient responsible for this data MINNEAPOLIS
State Zip Code+4 Congressional District
MN 55455 5
Country  
US

Recipient Highly Compensated Officers
Prime Recipient Indication of Reporting Applicability # Officer Name Officer Compensation
Recipient responsible for this data 1 Recipient responsible for this data Recipient responsible for this data
2 Recipient responsible for this data Recipient responsible for this data
3 Recipient responsible for this data Recipient responsible for this data
4 Recipient responsible for this data Recipient responsible for this data
5 Recipient responsible for this data Recipient responsible for this data

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USE IN THE RECIPIENT REPORT

The information provided by this tool is baseline data that the Recipient should include in the Recipient Report that must be submitted to FederalReporting.gov beginning October 1, 2009. The data from this tool can be cut and pasted directly into the Recipient Report.