The autoimmune response induced by α-synuclein peptides drives neuronal cell death and glial cell activation.

J Autoimmun

Division of Rheumatology. Department of Internal Medicine, Gyeongsang National University Hospital, Jinju 52727, Republic of Korea; Department of Convergence Medical Science, College of Medicine, Gyeongsang National University, Jinju 52727, Republic of Korea; Department of Internal Medicine, College of Medicine, Gyeongsang National University Hospital, Jinju 52727, Republic of Korea. Electronic address:

Published: July 2024

Parkinson's disease (PD) is a progressive neurodegenerative disorder associated with the loss of dopaminergic neurons and neuroinflammation. Recent studies have identified a role of T cells in the pathogenesis of PD. Additionally, these studies suggested that α-synuclein (α-Syn) is related to abnormal T-cell responses and may act as an epitope and trigger autoimmune T-cell responses. However, it is unclear whether the α-Syn-mediated autoimmune response occurs and whether it is related to neuronal cell death and glial cell activation. In this study, we investigated the autoimmune T-cell response induced by α-Syn peptides and evaluated the neurotoxic effect of the α-Syn peptide-mediated autoimmune response. The immunization of mice with α-Syn peptides resulted in enhanced autoimmune responses, such as the peptide recall response, polarization toward Th1/Th17 cells, and regulatory T cell imbalance. Furthermore, the α-Syn autoimmune response led to the death of primary neurons cocultured with splenocytes. Treatment with conditioned media from α-Syn peptide-immunized splenocytes induced microglia and toxic A1-type astrocyte activation. Taken together, our results provide evidence of the potential role of the α-Syn-initiated autoimmune response and its contribution to neuronal cell death and glial cell activation.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jaut.2024.103256DOI Listing

Publication Analysis

Top Keywords

autoimmune response
20
neuronal cell
12
cell death
12
death glial
12
glial cell
12
cell activation
12
autoimmune
8
response induced
8
t-cell responses
8
autoimmune t-cell
8

Similar Publications

Angiogenesis is an intricate pathway that involves the formation of new blood capillaries from old, functioning ones. Improper angiogenesis is a feature of numerous maladies, including malignancy and autoimmune disorders. Indole-related derivatives are believed to interfere with the mitotic spindle, inhibiting the multiplication, and invasion of cancerous human cells.

View Article and Find Full Text PDF

Thymomas have been associated with the generation of paraneoplastic autoantibodies to neurogenic epitopes, collapsin-response-mediator protein-5 receptor (CRMP-5) and alpha-amino-3-hydroxyl-5methyl-4isoxazolepropionic acid receptor (AMPAR), in patients with acute viral infection. We report a patient with thymoma and myasthenia gravis, with SARS-CoV-2 infection, who became comatose secondary to autoimmune encephalitis. Plasmapheresis, high-dose steroids, pyridostigmine, eculizumab, and rituximab did not restore neurologic function.

View Article and Find Full Text PDF

The p38α-MK2 signaling axis plays an important role in the inflammatory response of cells. Here, we carried out a series of optimizations on CDD-450, aiming to enhance inhibition of the p38α-MK2 complex and improve pharmacokinetic properties. First, the magic F strategy was utilized to obtain compound , which displayed a 60-fold increase in tumor necrosis factor α inhibition and a 600-fold increase in interleukin-6 inhibition.

View Article and Find Full Text PDF

Introduction: Leucine-rich glioma-inactivated 1 (LGI-1) antibody encephalitis is a rare subtype of autoimmune limb encephalitis (ALE), which is marked by rapid neuropsychiatric decline. This report details a comprehensive approach to its diagnosis and management.

Assessment: In this case, a 68-year-old man presented with aggressive behaviors, cognitive decline, and seizure-like episodes.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!