ArticleClinical and experimental immunology2002
T-cell reactivity to glutamic acid decarboxylase in stiff-man syndrome and cerebellar ataxia associated with polyendocrine autoimmunity.
Article in Clinical and experimental immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- The limbic and extra-limbic encephalitis associated with glutamic acid decarboxylase (GAD)-65 antibodies: an observational study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Observational
- GAD antibodies in neurological disease: a critical evaluation of the utility and treatment implications of GAD antibodies in clinical practice.Journal of neurology · 2025Article
- Toward curing neurological autoimmune disorders: Biomarkers, immunological mechanisms, and therapeutic targets.Neuron · 2025Review
- Neurological Diseases and Prevalence of Antineuronal Antibodies in Patients with Autoimmune Polyendocrine Syndrome Type 1 - A National Cohort Study.Journal of clinical immunology · 2024Article
- Novelties in Autoimmune and Paraneoplastic Cerebellar Ataxias: Twenty Years of Progresses.Cerebellum (London, England) · 2022Review
- Primary DQ effect in the association between HLA and neurological syndromes with anti-GAD65 antibodies.Journal of neurology · 2020Article
- GAD antibodies in neurological disorders - insights and challenges.Nature reviews. Neurology · 2020Review
- Associations between HLA and autoimmune neurological diseases with autoantibodies.Auto- immunity highlights · 2020Review
- Immune-mediated Cerebellar Ataxias: Practical Guidelines and Therapeutic Challenges.Current neuropharmacology · 2019Review
- Acute Cerebellar Ataxia Associated with Anti-glutamic Acid Decarboxylase Antibodies Mimicking Miller Fisher Syndrome.Internal medicine (Tokyo, Japan) · 2018Article
- Management of Autoimmune Encephalitis: An Observational Monocentric Study of 38 Patients.Frontiers in immunology · 2018Observational
- Cerebellar disease associated with anti-glutamic acid decarboxylase antibodies: review.Journal of neural transmission (Vienna, Austria : 1996) · 2017Review
- Expanding Role of T Cells in Human Autoimmune Diseases of the Central Nervous System.Frontiers in immunology · 2017Review
- Consensus Paper: Neuroimmune Mechanisms of Cerebellar Ataxias.Cerebellum (London, England) · 2016Review
- Glycine receptor antibodies in PERM and related syndromes: characteristics, clinical features and outcomes.Brain : a journal of neurology · 2014Article
- Central nervous system destruction mediated by glutamic acid decarboxylase-specific CD4+ T cells.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Characterization of CD4+ T cells specific for glutamic acid decarboxylase (GAD65) and proinsulin in a patient with stiff-person syndrome but without type 1 diabetes.Diabetes/metabolism research and reviews · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibodies to glutamic acid decarboxilase (GAD-Abs) are present in the serum of 60-80% of newly diagnosed type 1 diabetes (DM1) patients and patients with autoimmune polyendocrine syndrome (APS) associated with DM1. Higher titre of GAD-Abs are also present in the serum of 60% of patients with stiff-man syndrome (SMS) and all reported patients with cerebellar ataxia associated with polyendocrine autoimmunity (CAPA). Several studies suggest that GAD-Abs may play a critical role in the pathogenesis of SMS and CAPA but little is known about T-cell responsiveness to GAD-65 in these neurological diseases. To analyse cell-mediated responses to GAD, we studied the peripheral blood lymphocyte proliferation and cytokine responses to recombinant human GAD-65 in 5 patients with SMS, 6 with CAPA, 9 with DM1, 8 with APS and 15 control subjects. GAD-65-specific cellular proliferation was significantly higher in SMS than in CAPA, DM1, APS or controls. In contrast, only T cells from CAPA patients showed a significantly high production of interferon-gamma after GAD stimulation, compared to all other patients and controls. No differences were found for IL-4 production. These results suggest that, despite similar humoral autoreactivity, cellular responses to GAD are different between SMS and CAPA, with a greater inflammatory response in CAPA, and this difference may be relevant to the pathogenesis of these diseases.
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