ReviewFrontiers in immunology2017
NLR-Dependent Regulation of Inflammation in Multiple Sclerosis.
Review in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 92 citations in OpenAlex.
- Ubiquitination-mediated degradation of NLRX1 drives metabolic vulnerability and accelerates intervertebral disc degeneration.Cell death and differentiation · 2026Article
- Role of Nod-like Receptors inMicroorganisms · 2026Review
- Beyond relapses: How BTK inhibitors are shaping the future of progressive MS treatment.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Differences of the 6N and 6J Substrains of C57BL/6 Mice in the Development of Experimental Autoimmune Encephalomyelitis.MedComm · 2025Article
- Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Inflammation in Metal-Induced Neurological Disorders and Neurodegenerative Diseases.Biological trace element research · 2024Review
- Impact of Ionizing Radiation Exposure on Placental Function and Implications for Fetal Programming.International journal of molecular sciences · 2024Review
- Bioinformatics analysis and experimental verification of NLRX1 as a prognostic factor for esophageal squamous cell carcinoma.Oncology letters · 2024Article
- NLRX1 Inhibits LPS-Induced Microglial Death via Inducing p62-Dependent HO-1 Expression, Inhibiting MLKL and Activating PARP-1.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Impact of Microbiome-Brain Communication on Neuroinflammation and Neurodegeneration.International journal of molecular sciences · 2023Review
- Sulfur-Element containing metabolic pathways in human health and crosstalk with the microbiome.Biochemistry and biophysics reports · 2023Review
- IL-11 induces NLRP3 inflammasome activation in monocytes and inflammatory cell migration to the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Microbiota and Glucidic Metabolism: A Link with Multiple Aspects and Perspectives.International journal of molecular sciences · 2023Review
- Altered Lnc-EGFR, SNHG1, and LincRNA-Cox2 Profiles in Patients with Relapsing-Remitting Multiple Sclerosis: Impact on Disease Activity and Progression.Diagnostics (Basel, Switzerland) · 2023Article
- Immune Cell Ratios Are Higher in Bipolar Affective than Unipolar Depressive Disorder and Modulated by Mood Episode: A Retrospective, Cross-Sectional Study.Brain sciences · 2023Article
- Glia Connect Inflammation and Neurodegeneration in Multiple Sclerosis.Neuroscience bulletin · 2023Review
- IRAK-M suppresses the activation of microglial NLRP3 inflammasome and GSDMD-mediated pyroptosis through inhibiting IRAK1 phosphorylation during experimental autoimmune encephalomyelitis.Cell death & disease · 2023Article
- The Role of Gut Dysbiosis and Potential Approaches to Target the Gut Microbiota in Multiple Sclerosis.CNS drugs · 2023Review
- Periventricular Microglia Polarization and Morphological Changes Accompany NLRP3 Inflammasome-Mediated Neuroinflammation after Hypoxic-Ischemic White Matter Damage in Premature Rats.Journal of immunology research · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) associated with inappropriate activation of lymphocytes, hyperinflammatory responses, demyelination, and neuronal damage. In the past decade, a number of biological immunomodulators have been developed that suppress the peripheral immune responses and slow down the progression of the disease. However, once the inflammation of the CNS has commenced, it can cause serious permanent neuronal damage. Therefore, there is a need for developing novel therapeutic approaches that control and regulate inflammatory responses within the CNS. Nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are intracellular regulators of inflammation expressed by many cell types within the CNS. They redirect multiple signaling pathways initiated by pathogens and molecules released by injured tissues. NLR family members include positive regulators of inflammation, such as NLRP3 and NLRC4 and anti-inflammatory NLRs, such as NLRX1 and NLRP12. They exert immunomodulatory effect at the level of peripheral immune responses, including antigen recognition and lymphocyte activation and differentiation. Also, NLRs regulate tissue inflammatory responses. Understanding the molecular mechanisms that are placed at the crossroad of innate and adaptive immune responses, such as NLR-dependent pathways, could lead to the discovery of new therapeutic targets. In this review, we provide a summary of the role of NLRs in the pathogenesis of MS. We also summarize how anti-inflammatory NLRs regulate the immune response within the CNS. Finally, we speculate the therapeutic potential of targeting NLRs in MS.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.