ArticleFrontiers in immunology2021
CX3CR1 But Not CCR2 Expression Is Required for the Development of Autoimmune Peripheral Neuropathy in Mice.
Article in Frontiers in immunology, 2021. 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 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Tissue-Resident Macrophage PIEZO1 Transduces Mechanical Stress into Inflammatory Pain in Acute Gout.Neuroscience bulletin · 2026Article
- An Examination of the Role of CX3CR1 in the Pathobiology of Degenerative Cervical Myelopathy: Evidence from Human and Mouse Tissue.Journal of clinical medicine · 2025Article
- Cannabinoid receptor 2 facilitates the Schwann cells-dependent peripheral nerve regeneration.Clinical and translational medicine · 2025Article
- White Matter Anomaly Associated Cognitive Impairment During Systemic Inflammation Is Related to CX3CR1 Mediated Microglia-Node Interactions That Impacts the Conductive Function of Axons.Journal of inflammation research · 2025Article
- Differential regulation of tissue-resident and blood-derived macrophages in models of autoimmune and traumatic peripheral nerve injury.Frontiers in immunology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
One hallmark of Guillain-Barre syndrome (GBS), a prototypic autoimmune peripheral neuropathy (APN) is infiltration of leukocytes (macrophages and T cells) into peripheral nerves, where chemokines and their receptors play major roles. In this study, we aimed to understand the potential contribution of chemokine receptors CCR2 and CX3CR1 in APN by using a well-established mouse model, B7.2 transgenic (L31) mice, which possesses a predisposed inflammatory background. We crossbred respectively CCR2KO and CX3CR1KO mice with L31 mice. The disease was initiated by partial ligation on one of the sciatic nerves. APN pathology and neurological function were evaluated on the other non-ligated sciatic nerve/limb. Our results revealed that L31/CX3CR1KO but not L31/CCR2KO mice were resistant to APN. CX3CR1 is needed for maintaining circulating monocyte and CD8
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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.