ArticleBMC immunology2003
Severe anaphylactic reactions to glutamic acid decarboxylase (GAD) self peptides in NOD mice that spontaneously develop autoimmune type 1 diabetes mellitus.
Article in BMC immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 57 citations in OpenAlex.
- Vaccine to Nano-Vaccine: Novel Technique to Treat Rheumatoid Arthritis.Current rheumatology reviews · 2025Review
- Soluble antigen arrays provide increased efficacy and safety over free peptides for tolerogenic immunotherapy.Frontiers in immunology · 2024Article
- Soluble Antigen Arrays Efficiently Deliver Peptides and Arrest Spontaneous Autoimmune Diabetes.Diabetes · 2021Article
- Rheumatoid arthritis vaccine therapies: perspectives and lessons from therapeutic ligand epitope antigen presentation system vaccines for models of rheumatoid arthritis.Expert review of vaccines · 2015Review
- Long-term silencing of autoimmune diabetes and improved life expectancy by a soluble pHLA-DR4 chimera in a newly-humanized NOD/DR4/B7 mouse.Human vaccines & immunotherapeutics · 2014Article
- Destabilization of peptide:MHC interaction induces IL-2 resistant anergy in diabetogenic T cells.Journal of autoimmunity · 2013Article
- LEAPS therapeutic vaccines as antigen specific suppressors of inflammation in infectious and autoimmune diseases.Journal of vaccines & vaccination · 2012Article
- Antigen-specific blocking of CD4-specific immunological synapse formation using BPI and current therapies for autoimmune diseases.Medicinal research reviews · 2012Review
- Article
- Dominant role of antigen dose in CD4+Foxp3+ regulatory T cell induction and expansion.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Suppression of ongoing T cell-mediated autoimmunity by peptide-MHC class II dimer vaccination.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Prophylactic and therapeutic suppression of experimental autoimmune encephalomyelitis by a novel bifunctional peptide inhibitor.Clinical immunology (Orlando, Fla.) · 2008Article
- Human alpha 1-antitrypsin therapy induces fatal anaphylaxis in non-obese diabetic mice.Clinical and experimental immunology · 2008Article
- Peptide-based immunotherapy of experimental autoimmune encephalomyelitis without anaphylaxis.European journal of immunology · 2007Article
- Hydrodynamic vaccination with DNA encoding an immunologically privileged retinal antigen protects from autoimmunity through induction of regulatory T cells.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
- Genetic deletion of a single immunodominant T-cell response confers susceptibility to virus-induced demyelination.Brain pathology (Zurich, Switzerland) · 2007Article
- Regulatory T cells in human disease and their potential for therapeutic manipulation.Immunology · 2006Review
- Reversing the defective induction of IL-10-secreting regulatory T cells in glucocorticoid-resistant asthma patients.The Journal of clinical investigation · 2006Article
- Specific antigen vaccination to treat autoimmune disease.Proceedings of the National Academy of Sciences of the United States of America · 2004Review
- Animal models have little to teach us about type 1 diabetes: 1. In support of this proposal.Diabetologia · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInsulin dependent (i.e., "type 1") diabetes mellitus (T1DM) is considered to be a T cell mediated disease in which TH1 and Tc autoreactive cells attack the pancreatic islets. Among the beta-cell antigens implicated in T1DM, glutamic acid decarboxylase (GAD) 65 appears to play a key role in the development of T1DM in humans as well as in non-obese diabetic (NOD) mice, the experimental model for this disease. It has been shown that shifting the immune response to this antigen from TH1 towards TH2, via the administration of GAD65 peptides to young NOD mice, can suppress the progression to overt T1DM. Accordingly, various protocols of "peptide immunotherapy" of T1DM are under investigation. However, in mice with experimental autoimmune encephalomyelitis (EAE), another autoimmune TH1 mediated disease that mimics human multiple sclerosis, anaphylactic shock can occur when the mice are challenged with certain myelin self peptides that initially were administered with adjuvant to induce the disease.
resultsHere we show that NOD mice, that spontaneously develop T1DM, can develop fatal anaphylactic reactions upon challenge with preparations of immunodominant GAD65 self peptides after immunization with these peptides to modify the development of T1DM.
conclusionsThese findings document severe anaphylaxis to self peptide preparations used in an attempt to devise immunotherapy for a spontaneous autoimmune disease. Taken together with the findings in EAE, these results suggest that peptide therapies designed to induce a TH1 to TH2 shift carry a risk for the development of anaphylactic reactivity to the therapeutic peptides.
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.