ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
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- Vascular Considerations for Amyloid Immunotherapy.Current neurology and neuroscience reports · 2022Review
- Whole-body senescent cell clearance alleviates age-related brain inflammation and cognitive impairment in mice.Aging cell · 2021Article
- Peripheral Markers of Vascular Endothelial Dysfunction Show Independent but Additive Relationships with Brain-Based Biomarkers in Association with Functional Impairment in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2021Article
- Vaccines targeting the primary amino acid sequence and conformational epitope of amyloid-β had distinct effects on neuropathology and cognitive deficits in EAE/AD mice.British journal of pharmacology · 2020Article
- Piperlongumine Improves Lipopolysaccharide-Induced Amyloidogenesis by Suppressing NF-KappaB Pathway.Neuromolecular medicine · 2018Article
- The role of neutrophil granule proteins in neuroinflammation and Alzheimer's disease.Journal of neuroinflammation · 2018Review
- Functional morphology of the blood-brain barrier in health and disease.Acta neuropathologica · 2018Review
- The blood-brain barrier in Alzheimer's disease.Neurobiology of disease · 2017Review
- T Lymphocytes and Inflammatory Mediators in the Interplay between Brain and Blood in Alzheimer's Disease: Potential Pools of New Biomarkers.Journal of immunology research · 2017Review
- Interaction of astrocytes and T cells in physiological and pathological conditions.Brain research · 2015Review
- Migration of blood cells to β-amyloid plaques in Alzheimer's disease.Experimental gerontology · 2015Review
- Prominence of central sphingosine-1-phosphate receptor-1 in attenuating aβ-induced injury by fingolimod.Journal of molecular neuroscience : MN · 2014Article
- CD4 T cells in immunity and immunotherapy of Alzheimer's disease.Immunology · 2013Review
- Prion-like propagation of protein aggregation and related therapeutic strategies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- Transgenic models for cytokine-induced neurological disease.Biochimica et biophysica acta · 2010Review
- T cells specifically targeted to amyloid plaques enhance plaque clearance in a mouse model of Alzheimer's disease.PloS one · 2010Article
- Transcriptomic and genetic studies identify IL-33 as a candidate gene for Alzheimer's disease.Molecular psychiatry · 2009Article
- Mechanism-based treatments for Alzheimer's disease.Dialogues in clinical neuroscience · 2009Review
- Cytokine-mediated inhibition of fibrillar amyloid-beta peptide degradation by human mononuclear phagocytes.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Immunotherapy targeting the amyloid beta (Abeta) peptide is a novel therapy under investigation for the treatment of Alzheimer's disease (AD). A clinical trial using Abeta(1-42) (AN1792) as the immunogen was halted as a result of development of meningoencephalitis in a small number of patients. The cytokine TGF-beta1 is a key modulator of immune responses that is increased in the brain in AD. We show here that local overexpression of TGF-beta1 in the brain increases both meningeal and parenchymal T lymphocyte number. Furthermore, TGF-beta1 overexpression in a mouse model for AD [amyloid precursor protein (APP) mice] leads to development of additional T cell infiltrates when mice were immunized at a young but not old age with AN1792. Notably, only mice overproducing both Abeta (APP mice) and TGF-beta1 experienced a rise in T lymphocyte number after immunization. One-third of infiltrating T cells were CD4 positive. We did not observe significant differences in B lymphocyte numbers in any of the genotypes or treatment groups. These results demonstrate that TGF-beta1 overproduction in the brain can promote T cell infiltration, in particular after Abeta(1-42) immunization. Likewise, levels of TGF-beta1 or other immune factors in brains of AD patients may influence the response to Abeta(1-42) immunization.
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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.