This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The body of evidence developed over the last 10 - 20 years suggests that type 1 diabetes (T1D) in humans is a chronic, slowly progressive autoimmune disease. The objective of this study is to identify immune intervention strategies that will prevent the progression of beta cell destruction from the time of onset of T1D. The persistence of at least some beta cells should improve long-term diabetes care and prevent not only complications of the disease itself but also hypoglycemia, which is a consequence of its management.
The aim i s to arrest beta cell destruction in newly diabetic subjects because immune modulation may not work well alone once the autoimmune process has progressed to complete or near complete destruction of beta cells. The study?s rationale is to demonstrate a meaningful preservation of islet function with minimal immune system side effects. The data from this clinical trial could serve as the basis for a larger trial if the results are sufficiently positive, or they could suggest other combined intervention trials that might achieve either better efficacy or potentially preserve C-peptide without the need for continued immunosuppression. An intervention, which could restore normal islet function and maintain production of insulin would significantly improve the prognosis for metabolic control of diabetes and thus reduce long-term complications. This study will also examine the effect of the proposed treatment on surrogate markers for immunologic effects and outcomes Modulation of the immune response could lower autoantibody titers and either reduce or prevent the generation of autoantigenic T-cell responses.

National Institute of Health (NIH)
National Center for Research Resources (NCRR)
General Clinical Research Centers Program (M01)
Project #
Application #
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of Florida
Internal Medicine/Medicine
Schools of Medicine
United States
Zip Code
Mangal, Naveen; James, Margaret O; Stacpoole, Peter W et al. (2018) Model Informed Dose Optimization of Dichloroacetate for the Treatment of Congenital Lactic Acidosis in Children. J Clin Pharmacol 58:212-220
Boissoneault, Jeff; Letzen, Janelle; Lai, Song et al. (2016) Abnormal resting state functional connectivity in patients with chronic fatigue syndrome: an arterial spin-labeling fMRI study. Magn Reson Imaging 34:603-8
Shumyak, Stepan; Yang, Li-Jun; Han, Shuhong et al. (2016) ""Lupoid hepatitis"" in SLE patients and mice with experimental lupus. Clin Immunol 172:65-71
Hendeles, Leslie; Khan, Yasmeen R; Shuster, Jonathan J et al. (2015) Omalizumab therapy for asthma patients with poor adherence to inhaled corticosteroid therapy. Ann Allergy Asthma Immunol 114:58-62.e2
Price, Catherine C; Levy, Shellie-Anne; Tanner, Jared et al. (2015) Orthopedic Surgery and Post-Operative Cognitive Decline in Idiopathic Parkinson's Disease: Considerations from a Pilot Study. J Parkinsons Dis 5:893-905
Krueger, Charlene A; Cave, Emily C; Garvan, Cynthia (2015) Fetal response to live and recorded maternal speech. Biol Res Nurs 17:112-20
Jones, Jacob D; Marsiske, Michael; Okun, Michael S et al. (2015) Latent growth-curve analysis reveals that worsening Parkinson's disease quality of life is driven by depression. Neuropsychology 29:603-9
Morishita, Takashi; Foote, Kelly D; Archer, Derek B et al. (2015) Smile without euphoria induced by deep brain stimulation: a case report. Neurocase 21:674-8
Del-Aguila, J L; Cooper-DeHoff, R M; Chapman, A B et al. (2015) Transethnic meta-analysis suggests genetic variation in the HEME pathway influences potassium response in patients treated with hydrochlorothiazide. Pharmacogenomics J 15:153-7
Del-Aguila, J L; Beitelshees, A L; Cooper-Dehoff, R M et al. (2014) Genome-wide association analyses suggest NELL1 influences adverse metabolic response to HCTZ in African Americans. Pharmacogenomics J 14:35-40

Showing the most recent 10 out of 266 publications