Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain.
Brain Behav Immun
January 2025
Laboratories of Neuroimmunology, Department of Symptom Research, University of Texas MD Anderson Cancer Center, Houston, USA. Electronic address:
Preclinical and clinical studies have established that autoreactive immunoglobulin G (IgG) can drive neuropathic pain. We recently demonstrated that sciatic nerve chronic constriction injury (CCI) in male and female mice results in the production of pronociceptive IgG, which accumulates around the lumbar region, including within the dorsal root ganglia (DRG) and spinal cord, facilitating the development of neuropathic pain. These data raise the intriguing possibility that neuropathic pain may be alleviated by reducing the accumulation of IgG.
View Article and Find Full Text PDFBiomarkers of Intrathecal Synthesis May Be Associated with Cognitive Impairment at MS Diagnosis.
Int J Mol Sci
January 2025
Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), Department of Health Sciences, University of Piemonte Orientale, 28100 Novara, Italy.
The pathophysiology of cognitive impairment (CI) in multiple sclerosis (MS) remains unclear. Meningeal B cell aggregates may contribute to cortical grey matter pathology. Cerebrospinal fluid (CSF), kappa free light chains (KFLC), and KFLCs-Index (kappa-Index) are reliable quantitative markers of intrathecal synthesis, but few data have been presented exploring the association with CI, and no data are present for lambda FLC (LFLC) in MS.
View Article and Find Full Text PDFIgG-NR2B-A Potentially Valuable Biomarker in the Management of Refractory Anti-NMDAR Encephalitis.
Int J Mol Sci
January 2025
Department of Pathology, Faculty of Health Care and Social Work, Trnava University and University Hospital, 917 02 Trnava, Slovakia.
The autoantibodies against the NR1 subunit are well known in the pathomechanism of NMDAR encephalitis. The dysfunction of the NR2 subunit could be a critical factor in this neurological disorder due to its important role in the postsynaptic pathways that direct synaptic plasticity. We report a case of paraneoplastic anti-NMDAR encephalitis presented alongside very severe illness.
View Article and Find Full Text PDFIntrathecal Immunoglobulin A Synthesis in Multiple Sclerosis: From Biological Aspects to Clinical Relevance.
Biomolecules
January 2025
Department of Neurology, Christian-Doppler University Hospital, Paracelsus Medical University, 5020 Salzburg, Austria.
Intrathecal immunoglobulin A (IgA) synthesis in multiple sclerosis (MS) has long earned little attention, despite a potential significance in disease pathogenesis and prognosis. The presence of IgA-positive plasma cells in MS lesions and along damaged axons suggests a role in disease pathogenesis. Available clinical evidence about a potential positive or negative prognostic role is scarce and inconclusive.
View Article and Find Full Text PDFElevated Kappa Index in the Absence of Cerebrospinal Fluid IgG Oligoclonal Bands: Contribution of Intrathecal IgM and IgA Synthesis.
Biomolecules
January 2025
Department of Biomedical, Metabolic and Neurosciences, University of Modena and Reggio Emilia, 41121 Modena, Italy.
The kappa index is a well-established marker of intrathecal synthesis (IS) of immunoglobulin (Ig). Routinely used for diagnostic aims, IgG IS, which can be assessed quantitatively (ad hoc formulas) or qualitatively (oligoclonal bands, OCBs), may fail in detecting a humoral immune response within the central nervous system (CNS). The main aim of this study was to evaluate the kappa index for its ability to detect the presence of CNS humoral immunity and to associate it with a distinct group of disorders, in the absence of IgG IS/OCBs.
View Article and Find Full Text PDFWant 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!