Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Encephalitis ll: Pathophysiology

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

Encephalitis l: Introduction

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Acute and longitudinal magnetic resonance imaging abnormalities in antibody-mediated encephalitis.

Brain communications·2026

Same author

A Critical Review of Clinical Factors and Tools for Predicting Chimeric Antigen Receptor T-Cell Toxicities.

Transplantation and cellular therapy·2026

Same author

Cognitive Recovery Following Immune Effector Cell-Associated Neurotoxicity Syndrome in the First 6 Months after Chimeric Antigen Receptor T-Cell Therapy.

Transplantation and cellular therapy·2026

Same author

Characterising executive functioning in the chronic phase of autoimmune encephalitis: A study by the Australian autoimmune encephalitis consortium.

Multiple sclerosis and related disorders·2026

Same author

Study protocol for a mixed methods convergent investigation of family domestic and sexual violence in multiple sclerosis and broader neurology in Australia.

PloS one·2026

Same author

A Computerized Cognitive Test for Immune Effector Cell-Associated Neurotoxicity Syndrome in Chimeric Antigen Receptor T-Cell Therapy Recipients: A Pilot Study.

Transplantation and cellular therapy·2026

Search research articles

Related Experiment Video

Updated: May 21, 2026

Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis

Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis

Published on: December 1, 2023

Plasma proteome in LGI-1 autoimmune encephalitis.

Robb Wesselingh^1,2, Nabil Seery^3,4, Katherine Ko^3,4

¹Department of Neuroscience, School of Translational Medicine, Monash University, Melbourne, Australia. robb.wesselingh@monash.edu.

Journal of Neuroinflammation

|May 20, 2026

Summary

Leucine-rich glioma-inactivated antibody associated autoimmune encephalitis (LGI-1 AE) involves immune activation and complement cascade. This study reveals IL-6 signaling and suppressed autophagy as key mechanisms, suggesting new therapeutic targets for LGI-1 AE.

Keywords:

Autoimmune encephalitis Autophagy Biomarkers Complement IL-6 LGI-1 Proteomics Transcriptomics

More Related Videos

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis

Published on: June 2, 2022

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

Related Experiment Videos

Last Updated: May 21, 2026

Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis

Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis

Published on: December 1, 2023

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis

Published on: June 2, 2022

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

Area of Science:

Neuroimmunology
Proteomics
Transcriptomics

Background:

Leucine-rich glioma-inactivated antibody associated autoimmune encephalitis (LGI-1 AE) is a rare autoimmune disorder affecting the central nervous system, leading to seizures and cognitive impairment.
While immunotherapy can be effective, persistent cognitive deficits remain a challenge.
Previous research indicated peripheral immune cell abnormalities in chronic LGI-1 AE.

Purpose of the Study:

To investigate peripheral immune system alterations in acute and chronic LGI-1 AE.
To identify potential biomarkers and therapeutic targets by analyzing plasma proteomic and monocyte transcriptomic profiles.

Main Methods:

Plasma proteomic profiling using SomaLogic 11k panel on samples from acute LGI-1 AE, chronic LGI-1 AE, and healthy controls.
Monocyte bulk RNA sequencing from chronic LGI-1 AE patients and controls.
Differential expression analysis and pathway enrichment analysis (Gene Ontology Biological Processes).

Main Results:

Plasma proteomic analysis revealed significant upregulation of innate immune activation, myeloid cell chemoattractants, complement cascade components, and lymphocyte signaling molecules in acute LGI-1 AE.
Autophagy-related pathways were significantly downregulated in acute LGI-1 AE.
Monocyte transcriptomics highlighted IL-6 signaling as a key dysregulated pathway, with 18 upregulated and 170 downregulated genes.

Conclusions:

IL-6 signaling and terminal complement cascade activation are implicated in LGI-1 AE pathogenesis.
Suppressed autophagy pathways represent a potential novel mechanism contributing to LGI-1 AE, warranting further investigation.
These findings suggest opportunities for therapeutic repurposing and highlight the need for deeper understanding of autophagy's role in LGI-1 AE.