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Autoimmune Encephalitis (AE)

Autoimmune encephalitis (AE) refers to brain inflammation caused by abnormalities in the body's immune system and is typically considered reversible encephalitis caused by non-infectious factors. Diagnosis and therapy of this condition remain significant challenges. Our company offers drug development and therapeutic solutions specifically targeting AE, which are aimed at assisting you in achieving your research and development goals more rapidly and effectively.

Introduction to AE

AE is a central nervous system inflammatory disorder caused by an abnormal immune response to neuronal antigenic components. It predominantly involves damage to the central nervous system mediated by humoral or cellular immune reactions. AE accounts for approximately 10% to 20% of encephalitis cases, with an estimated annual incidence rate of around 1 in 100,000.

Pathogenesis of AE

The pathogenesis of AE is multifaceted and involves a complex interplay of immunological mechanisms targeting neuronal antigens. Emerging evidence from AE literature suggests that the disease onset is triggered by an aberrant immune response, often precipitated by preceding infections, tumors, or other environmental factors. This dysregulated immune response produces autoantibodies that recognize specific neuronal surface or synaptic proteins, such as NMDA receptors, LGI1, CASPR2, or GABAB receptors.

Upon breaching the blood-brain barrier, these autoantibodies directly bind to their target antigens, resulting in dysregulation of synaptic transmission, neuronal excitability, and neuroinflammation. Additionally, complement-mediated mechanisms may further exacerbate tissue damage and inflammatory responses within the central nervous system (CNS).

Fig.1 The functional network changes of NMDAR encephalitis.Fig.1 The functional network changes of NMDAR encephalitis. (Heine, J., et al., 2023)

Diagnostics Development of AE

In the advancement of diagnostic techniques for AE, the detection of specific autoantibodies or biomarkers, such as NMDA receptor antibodies or LGI1 antibodies, is achieved through methodologies like enzyme-linked immunosorbent assay (ELISA) and immunofluorescence assay (IFA), which are subsequently validated. Cell-based assays, including live neuronal cell testing and transfected cell lines expressing target antigens, are advancing to provide more accurate diagnostic tools.

Therapy Development of AE

Monoclonal Antibodies

The advancement of monoclonal antibody therapy for AE encompasses the generation of antibodies designed to selectively target neuronal antigens associated with the condition, such as NMDA receptors or LGI1 proteins. For example, the monoclonal antibody rituximab, which targets CD20 on B-cells, has shown promise in the therapy of AE by depleting autoantibody-producing cells and modulating the immune response.

Cell Therapies

The progress of cell therapy for AE revolves around the exploration of methodologies rooted in stem cell-based techniques, such as mesenchymal stem cells (MSCs) or neural progenitor cells (NPCs), for their potential in modulating the immune response and promoting neural regeneration in AE individuals. Studies are assessing the safety and efficacy of these cell therapies in animal models of AE, with promising results indicating their potential for translation.

Our Services

Our company is committed to seamlessly integrating teams in biotechnology, pharmaceuticals, and medical devices.Our expertise provides a reliable framework for drug and therapy development, ensuring a smooth journey for your research endeavors.

Platforms of AE Therapy Development

Animal Models of AE

We have established expertise in developing and utilizing relevant animal models that closely mimic the disease characteristics and response to therapy. These models enable us to evaluate the safety and efficacy of potential therapies.

Induced Animal Models
Our company specializes in developing induced animal models that faithfully replicate AE's pathology and immunological features. Experimental Autoimmune Encephalomyelitis (EAE) induces immune responses by immunizing animals with myelin proteins like MOG or MBP, mimicking AE symptoms. The antibody transfer model transfers specific antibodies from AE patients or animals, triggering neuroinflammation akin to AE's pathology.
Optional Models
  • MOG-Induced Model
  • NMDA Receptor Antibody Transfer Model
Genetically Engineered Models
Our expertise in genetic engineering techniques, such as CRISPR/Cas9 technology, allows us to generate accurate and reliable models that recapitulate the genetic alterations observed in human AE.
Optional Models
  • Myelin Oligodendrocyte Glycoprotein (MOG) Overexpressed Model
  • T-Cell Receptor (TCR) Transgenic Model
  • Immune Regulatory Genes Conditional Knockout Model
  • Interleukin-17 (IL-17) Overexpress Model
Optional Species Mice, Rats, Others

In addition to these models, our comprehensive services encompass other models that target specific signaling pathways and molecular targets. These models have provided valuable insights into the pathogenesis of AE and identify potential therapeutic targets and strategies.

If you are considering utilizing our services, we welcome you to contact us at your convenience to discuss how we can best meet your needs and support your goals.


  • Heine, J., et al., "Autoimmune encephalitis-An update. "Nervenarzt (2023). 94(6): p. 525-537.
  • Varley, J.A., et al., "Autoimmune encephalitis: recent clinical and biological advances." J Neurol (2023). 270(8): p. 4118-4131.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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