Νικόλαος Xηνάς​​

 

https://doi.org/10.3389/fimmu.2025.1604174 ​​​

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​REVIEW

Front. Immunol., 18 July 2025

Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders

Volume 16 - 2025 | https://doi.org/10.3389/fimmu.2025.1604174

CAR T-cells meet autoimmune neurological diseases: a new dawn for therapy

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Nikolaos A. Chinas * †       Harry Alexopoulos * †

Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece

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Abstract

Autoimmunity and autoimmune diseases arise when the immune system erroneously targets self-antigens leading to tissue damage. Consequently, immunomodulatory and mainly immunosuppressive drugs comprise the conventional treatment in conditions such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. However, many of these agents often fall short of providing a cure and have a limit on symptom management. This underscores the urgent need for even more advanced therapies for patients to constrain progressive disability. Therefore, currently, researchers explore the potential of chimeric antigen receptor (CAR) T-cell therapy for autoimmune diseases considering its success in cancer treatment and specifically in hematological malignancies. This review will examine recent advancements in CAR T-cell therapy for autoimmune disorders, highlighting how CAR T cells can be engineered to precisely target and eliminate autoreactive immune cells that drive these debilitating diseases, particularly those affecting the nervous system such as Multiple sclerosis, Myasthenia gravis, Neuromyelitis optica, Stiff-person syndrome, Autoimmune encephalitis, MOG-antibody disease and Chronic inflammatory demyelinating polyneuropathy. Also, through an analysis of preclinical and clinical data, we will assess the efficacy, safety, potential side effects and limitations of these innovative therapies. Lastly, we will underline the transformative potential of CAR T-cells in Autoimmune Neurology, offering a promising new hope for treatment where conventional therapies have failed.

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https://doi.org/10.1007/s10571-026-01784-w 

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Glutamate, Immune Cells and Alzheimer’s Disease

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Abstract

Glutamate (Glu), although the main excitatory neurotransmitter (NT) of the central nervous system (CNS), evidence recognizes its role in influencing immune cell function and activation, including cytokine production, cell proliferation, migration, and survival. Importantly, dysregulation of Glu homeostasis has been implicated in the pathogenesis of Alzheimer’s disease (AD), a neurodegenerative disorder characterized by progressive cognitive decline, neuronal loss and neuroinflammation. This review synthesizes current evidence on the biochemistry of the glutamatergic synapse, as well as the expression and signaling of Glu receptors (GluRs) in human immune cells. Furthermore, it examines two major hypotheses of AD pathogenesis —the glutamatergic and the neuroimmune hypothesis— and proposes a unified glutamatergic–neuroimmune framework. In this model, disrupted glutamatergic signaling at the neuron–glia–immune interface may represent a central contributor to AD pathology. Understanding the glutamatergic–neuroimmune axis may provide novel insights into therapeutic strategies targeting neuroimmune modulation in AD.

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Author information

Authors and Affiliations

1. Department of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece

   Nikolaos A. Chinas & Harry Alexopoulos

2. Department of Genetics, Microbiology and Statistics, Institut de Biomedicina de la Universitat de Barcelona (IBUB), Universitat de Barcelona, Barcelona, Spain

   Nikolaos A. Chinas

Corresponding authors

Correspondence to Nikolaos A. Chinas or Harry Alexopoulos.

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