ReviewJournal of internal medicine2011
Vaccination against type 1 diabetes.
Review in Journal of internal medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Vaccine for Diabetes-Where Do We Stand?International journal of molecular sciences · 2022Review
- Expression of recombinant glutamic acid decarboxylase in insect larvae and its application in an immunoassay for the diagnosis of autoimmune diabetes mellitus.Scientific reports · 2019Article
- Article
- Latent autoimmune diabetes of the adult: current knowledge and uncertainty.Diabetic medicine : a journal of the British Diabetic Association · 2015Review
- Comparative analysis of different biofactories for the production of a major diabetes autoantigen.Transgenic research · 2014Article
- Immune therapy in type 1 diabetes mellitus.Nature reviews. Endocrinology · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The clinical onset of type 1 diabetes or autoimmune diabetes occurs after a prodrome of islet autoimmunity. The warning signals for the ensuing loss of pancreatic islet beta cells are autoantibodies against insulin, GAD65, IA-2 and ZnT8, alone or in combinations. Autoantibodies against, for example, insulin alone have only a minor risk of type 1 diabetes. However, progression to clinical onset is increased by the induction of multiple islet autoantibodies. At the time of clinical onset, insulitis may be manifest, which seems to reduce the efficacy of immunosuppression. Autoantigen-specific immunotherapy with alum-formulated GAD65 (Diamyd(®)) shows promise to reduce the loss of beta-cell function after the clinical onset of type 1 diabetes. The mechanisms are unclear but may involve the induction of T regulatory cells, which may suppress islet autoantigen reactivity. Past and ongoing clinical trials have been safe. Future clinical trials, perhaps as combination autoantigen-specific immunotherapy, may increase the efficacy in preventing the clinical onset in subjects with islet autoantibodies or preserve residual beta-cell function in patients newly diagnosed with type 1 diabetes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.