PMID- 21524383 OWN - NLM STAT- MEDLINE DCOM- 20110930 LR - 20211020 IS - 1944-7930 (Electronic) IS - 1539-6509 (Print) IS - 1539-6509 (Linking) VI - 11 IP - 59 DP - 2011 Apr TI - Autoantigen based vaccines for type 1 diabetes. PG - 293-301 AB - Type 1 diabetes is an organ-specific autoimmune disease caused by chronic inflammation (insulitis), which damages the insulin producing beta-cells of the pancreatic Islets of Langerhans. Dendritic cells (DCs) are generally the first cells of the immune system to process beta-cell autoantigens and, by promoting autoreactivity, play a major role in the onset of insulitis. Although no cure for diabetes presently exists, the onset of insulitis can be diminished in the non-obese diabetic (NOD) mouse type 1 diabetes model by inoculation with endogenous beta-cell autoantigens. These include the single peptide vaccines insulin, GAD(65) (glutamic acid decarboxylase), and DiaPep277 (an immunogenic peptide from the 60-kDa heat shock protein). DiaPep277 is the only autoantigen so far to demonstrate positive results in human clinical trials. Diamyd (an alum adjuvant + recombinant GAD(65) protein formulation) has shown great promise for suppressing beta-cell autoreactivity in phase I and II clinical trials. While Diamyd preserved residual insulin secretion in early-onset type 1 diabetes patients, it did not reduce the amounts of insulin required to maintain euglycemia. Recently, multi-component vaccines composed of the anti-inflammatory cytokine (IL-10) and insulin or GAD(55) linked to an immunostimulatory molecule, the cholera toxin B subunit, were shown to safely and completely inhibit diabetes onset in NOD mice. This result suggests that multi-component vaccine strategies are promising for prevention and reversal of diabetes autoimmunity in humans. Here we focus on the development of autoantigen vaccines for type 1 diabetes and demonstrate that multi-component vaccines are promising candidates for type 1 diabetes clinical studies. FAU - Nicholas, Dequina AU - Nicholas D AD - Center for Health Disparities and Molecular Medicine, Department of Biochemistry, Loma Linda University School of Medicine, California 92354, USA. FAU - Odumosu, Oludare AU - Odumosu O FAU - Langridge, William H R AU - Langridge WH LA - eng GR - F31 GM101961/GM/NIGMS NIH HHS/United States GR - R21 DK063576/DK/NIDDK NIH HHS/United States PT - Journal Article PT - Review PL - United States TA - Discov Med JT - Discovery medicine JID - 101250006 RN - 0 (Autoantigens) RN - 0 (Peptides) RN - 0 (Vaccines) SB - IM MH - Animals MH - Autoantigens/*immunology MH - Dendritic Cells/immunology MH - Diabetes Mellitus, Type 1/*immunology/pathology/*prevention & control MH - Humans MH - Immunotherapy MH - Peptides/immunology/therapeutic use MH - Vaccines/*immunology PMC - PMC6474774 MID - NIHMS438281 COIS- Disclosure The authors report no conflicts of interest. EDAT- 2011/04/29 06:00 MHDA- 2011/10/01 06:00 PMCR- 2019/04/19 CRDT- 2011/04/29 06:00 PHST- 2011/04/29 06:00 [entrez] PHST- 2011/04/29 06:00 [pubmed] PHST- 2011/10/01 06:00 [medline] PHST- 2019/04/19 00:00 [pmc-release] PST - ppublish SO - Discov Med. 2011 Apr;11(59):293-301.