Three Projects and two Cores within this P01 receive support by the now well-established Core A. Based on our two decades of experience with such oversight, we believe the notion of ?success? for the overall program depends on the P01 having an effective Administrative Core component as a central element of fiscal/regulatory coordination, human subject recruitment, and scientific guidance/external evaluation. With this belief, the four goals of Core A are as follows: 1) Coordinate the budgetary and fiscal aspects of the program. The proposed program involves direct cost disbursements to investigators of Projects 1, 2, & 3, as well as Cores A and B; hence, careful oversight represents an absolute administrative requirement. 2) Facilitate communication among investigators within the program.
This aim takes a pragmatic form through Core A's implementation of a variety of functions ranging from organizing regularly scheduled meetings between program investigators to training of Project investigators by the program's Cores. 3) Coordinate, as a Program Executive Committee, ongoing feedback with regard to the directions of the individual Projects and Cores, the goals and activities of the P01, and respond to input provided by the External Advisory Board ? individuals who provide on-site visits to the University of Florida as well as teleconference based reviews ? for the purpose of maximizing both the progress and success of the program. 4) Organize the collection of human materials, generate appropriate data sets, provide statistical support to the program, assure compliance with appropriate regulatory bodies and edicts (e.g., Institutional Review Board, Health Insurance Portability and Accountability Act), and facilitate communication of program results. In addition to the aforementioned functions, the administrative staff of the program will also be responsible for communication with the NIH staff, as well as for assistance with publications and presentation of program results. It should be noted that the P01's Program Executive Committee has reviewed changing priorities and advances in the field of type 1 diabetes (T1D) and with this renewal application, organized itself to address the growing needs for: 1) identifying key processes at the intersection of ?-cell biology and anti-?-cell immunity; 2) understanding genotype/phenotype interactions in T1D that impact immune responsiveness; 3) developing improved biomarkers (immune/metabolic/genetic) reflective of key pathogenic processes; and 4) discovering methods that would impart immune modification capable of preventing/reversing T1D. Directed/collaborative activities to achieve these goals, taken together with the successful completion of these P01 studies, should continue to prove beneficial for improving our understanding of the immunological and genetic contributions critical to the pathogenesis of T1D, identifying immune/genetic markers that enhance our ability to monitor the disorder's natural history and eventually, developing immunotherapies capable of preventing or reversing the disease.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
5P01AI042288-22
Application #
9944318
Study Section
Special Emphasis Panel (ZAI1)
Project Start
1997-09-30
Project End
2023-05-31
Budget Start
2020-06-01
Budget End
2021-05-31
Support Year
22
Fiscal Year
2020
Total Cost
Indirect Cost
Name
University of Florida
Department
Type
DUNS #
969663814
City
Gainesville
State
FL
Country
United States
Zip Code
32611
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Chen, Yi-Guang; Mathews, Clayton E; Driver, John P (2018) The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future. Front Endocrinol (Lausanne) 9:51
Kusmartseva, Irina; Beery, Maria; Philips, Tiffany et al. (2018) Hospital time prior to death and pancreas histopathology: implications for future studies. Diabetologia 61:954-958
Hu, Ronghua; Xia, Chang-Qing; Butfiloski, Edward et al. (2018) Effect of high glucose on cytokine production by human peripheral blood immune cells and type I interferon signaling in monocytes: Implications for the role of hyperglycemia in the diabetes inflammatory process and host defense against infection. Clin Immunol 195:139-148
Smith, Mia J; Rihanek, Marynette; Wasserfall, Clive et al. (2018) Loss of B-Cell Anergy in Type 1 Diabetes Is Associated With High-Risk HLA and Non-HLA Disease Susceptibility Alleles. Diabetes 67:697-703
Ratiu, Jeremy J; Racine, Jeremy J; Hasham, Muneer G et al. (2017) Genetic and Small Molecule Disruption of the AID/RAD51 Axis Similarly Protects Nonobese Diabetic Mice from Type 1 Diabetes through Expansion of Regulatory B Lymphocytes. J Immunol 198:4255-4267
Delitto, Daniel; Delitto, Andrea E; DiVita, Bayli B et al. (2017) Human Pancreatic Cancer Cells Induce a MyD88-Dependent Stromal Response to Promote a Tumor-Tolerant Immune Microenvironment. Cancer Res 77:672-683
Posgai, Amanda L; Wasserfall, Clive H; Kwon, Kwang-Chul et al. (2017) Plant-based vaccines for oral delivery of type 1 diabetes-related autoantigens: Evaluating oral tolerance mechanisms and disease prevention in NOD mice. Sci Rep 7:42372
Sebastiani, Guido; Ventriglia, Giuliana; Stabilini, Angela et al. (2017) Regulatory T-cells from pancreatic lymphnodes of patients with type-1 diabetes express increased levels of microRNA miR-125a-5p that limits CCR2 expression. Sci Rep 7:6897
O'Kell, Allison L; Wasserfall, Clive; Catchpole, Brian et al. (2017) Comparative Pathogenesis of Autoimmune Diabetes in Humans, NOD Mice, and Canines: Has a Valuable Animal Model of Type 1 Diabetes Been Overlooked? Diabetes 66:1443-1452

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