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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: THE ROLE OF CD5 IN B-CELL DEVELOPMENT AND AUTOIMMUNITY
UNIVERSITY OF ALABAMA AT BIRMINGHAM
DUNS Number: 063690705
UAB STATION, CBB 990
BIRMINGHAM, AL 35294
Recipient Report: Grant or Loan
Prime Recipient

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Reporting Information
Award Type Award Number Final Report
Grant 3R01AI076562-03S2 Recipient responsible for this data

Award Recipient Information
Recipient DUNS Number Recipient Account Number Recipient Congressional District
063690705 Recipient responsible for this data 6

Award Information
Funding Agency Code Awarding Agency Code Award Date
7529 7529 06-29-2010
Amount of Award Sub Account Number for Program Source (TAS)  
$ 42,675 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
DESCRIPTION (provided by applicant): The B1a (CD5+) B-cells are the primary producers of natural antibodies that are self-reactive and polyreactive but usually non-pathogenic. However, in some circumstances, B1a B-cells contribute substantially to the immunopathogenesis of chronic systemic autoimmune diseases such as rheumatoid arthritis (RA), Sjogren's syndrome and systemic lupus erythematosus (SLE). B1a B-cells are a critical arm of the innate immune system and provides the first line of defense against a variety of bacterial and viral infections. The most prevalent B-cell malignancy, chronic lymphocytic leukemia (CLL) is CD5+ B-cell in origin. Curiously, HIV patients with progressive disease have paucity of CD5+ B-cells; in contrast, seropositive individuals with non-progressive disease have normal levels of B1a B-cells. This suggests the possibility that natural antibodies produced by CD5+ B-cells may be protective in HIV. The role of CD5 in the development, function and/or persistence of B1a B-cells remains an unresolved and controversial question. Since CD5 can negatively regulate signals initiated when the B-cell antigen receptor (BCR) is engaged by antigen, it is believed that its primary role in B1a B-cells is to control B-cell receptor activation from responding pathogenically to self antigen. However, this dogma is challenged by the fact that that CD5-/- mice do not develop spontaneous autoimmune disease. Our recent studies have led to that discovery that a major and probably dominant role of CD5, in addition to its inhibitory activity, is to promote survival. The survival activity of CD5 is mediated its unique interaction with CK2, a serine/threonine kinase that is a major positive regulator of multiple cellular prosurvival signaling cascades. In a counterpoint to the prosurvival activity mediated by activation of CK2, CD5 also has an immunoreceptor tyrosine inhibitory motif (ITIM) necessary for negative regulation of B-cell activation. The ITIM domain also provides prosurvival signals by attenuating B-cell activation and therefore activation-induced cell death. We suggest that CD5 regulates the B-cell response by two independent but complimentary pathways. To test this model, we have generated by gene targeting approach mice expressing CD5 with selective inability to activate the CD5-CK2 dependent prosurvival signaling cascade and mice lacking CD5-ITIM dependent negative regulatory activity. Using these unique animal models, and the new model we propose to develop, we will be in a position to (1) determine the role of CD5 in the development of B1a B-cells and its contribution to autoimmunity, (2) elucidate how CD5 regulates B-cell responses to T-independent antigens and T-dependent antigens and (3) dissect the molecular mechanism of CD5-dependent survival and inhibitory signals in normal B-cells. These studies using the novel animal models will enable us to resolve CD5 biology in B-cells. An important outcome of the proposed studies will be a major advancement in our understanding of regulatory pathways in innate B-cell responses to bacterial and viral pathogens and the development of targeting approaches for treatment of autoimmune diseases and leukemia. PUBLIC HEALTH RELEVANCE: CD5+ B-Cells (B1a) B-cells are important in innate immunity, shaping the adaptive immune repertoire and in the immunopathogenesis of autoimmune diseases. The role of CD5 in the development of B-cells has been extensively interrogated, but remains unresolved; the goal of this proposal is to fill this gap in our understanding.

Project Information
Project Name or
Project/Program Title
Project Status Total Federal Amount ARRA Funds
Received/Invoiced
THE ROLE OF CD5 IN B-CELL DEVELOPMENT AND 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
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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
UAB STATION, CBB 990 Not Available Recipient responsible for this data
Infrastructure City Infrastructure State Infrastructure ZIP Code+4
BIRMINGHAM AL 35294
Infrastructure Purpose and Rationale
Recipient responsible for this data

Primary Place of Performance
Street Address 1 Street Address 2 City
SHEL 305 Recipient responsible for this data BIRMINGHAM
State Zip Code+4 Congressional District
AL 352432182 7
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
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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.