Background: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) and has been known as T-cell mediated. However, the contribution of multiple cell types, notably natural killer (NK) cells, has also been reported.
Aim: To quantify circulating total NK cells and its subpopulations, CD56 dim and bright, and to characterize the functional phenotype and IFN-γ and TNF-α production in relapsing-remitting patients treated with IFN-β and in apparently healthy controls.
Results: CD56 NK cells were found to be the least represented subpopulation. In relapse patients, the frequencies of IFN-γ-producing NK cells and their subpopulations were significantly decreased. In remission patients, CD56 NK cells expressed high levels of HLA-DR and CD54.
Conclusion: These results suggest that remission RRMS patients, although in an inactive stage of MS, present circulating NK cells with an activation phenotype, supporting the idea that NK cells may be relevant mediators in the MS pathophysiology.
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http://dx.doi.org/10.1007/s13760-024-02488-y | DOI Listing |
J Neuroinflammation
January 2025
Department of Neurology, Division of Neuroimmunology, School of Medicine, Johns Hopkins University, Baltimore, MD, 21287, USA.
Chronic innate immune activation in the central nervous system (CNS) significantly contributes to neurodegeneration in progressive multiple sclerosis (MS). Using multiple experimental autoimmune encephalomyelitis (EAE) models, we discovered that NLRX1 protects neurons in the anterior visual pathway from inflammatory neurodegeneration. We quantified retinal ganglion cell (RGC) density and optic nerve axonal degeneration, gliosis, and T-cell infiltration in Nlrx1 and wild-type (WT) EAE mice and found increased RGC loss and axonal injury in Nlrx1 mice compared to WT mice in both active immunization EAE and spontaneous opticospinal encephalomyelitis (OSE) models.
View Article and Find Full Text PDFActa Neurol Belg
January 2025
Ziekenhuis Oost Limburg, Genk, Belgium.
With the increasing use of disease modifying therapies as treatment for multiple sclerosis, knowledge of the rare but possibly severe adverse events becomes increasingly important. We present a case of Varicella-Zoster virus associated vasculopathy in a young male multiple sclerosis patient, treated with dimethyl fumarate. We aim to address this rare but potentially deadly complication of varicella-Zoster virus infection and spread awareness about the increased risk in this patient population.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Multiple sclerosis (MS) unfavorably affects working capacity. The Comprehensive International Classification of Functioning, Disability and Health Core Set for MS (cICF-MS), issued by the World Health Organization, has not yet been extended to evaluate working capacity level (WCL). To evaluate the relative importance of cICF-MS categories in relation to WCL.
View Article and Find Full Text PDFRev Neurol (Paris)
January 2025
Clinical Neuroscience Centre, CIC_P1414 Inserm, University Hospital, Rennes, France. Electronic address:
Neurobiol Dis
January 2025
Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK S7K 0M7, Canada; Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, SK S7N 0X8, Canada. Electronic address:
RNA binding protein dysfunction is a pathogenic feature of multiple neurological diseases, including multiple sclerosis (MS). Neurodegeneration (the loss of, or damage to neurons and axons) is the primary driver of disease progression in MS. Herein, we utilized a novel, neuron-specific model of neurodegeneration by transducing primary mouse neurons with mutant forms of the RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) identified from MS patients, including one within the M9-nuclear localization sequence of hnRNP A1 (A1(P275S)) and a second in the prion-like domain of hnRNP A1 (A1(F263S)) to test the hypothesis that neuronal hnRNP A1 dysfunction drives neurodegeneration in MS.
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