The CNS role of Toll-like receptor 4 in innate neuroimmunity and painful neuropathy.

By F. Tanga, N. Nutile‐Mcmenemy, J. Deleo. Proceedings of the National Academy of Sciences of the United States of America, 2005

633 citations recorded by the source corpus.

Subfields: Immunology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/cc5a608f44d2957f6ebf58514819910b46db8232

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Citations in the corpus

Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, positive): “Peripheral nerve injury causes a massive activation of, and change in, glial cells in the spinal cord as well as infiltration of peripheral immune-competent cells, notably macrophages and T-cells.(38,317,360) The extent and duration of the changes in microglia and astrocytes is much”
Pathological and protective roles of glia in chronic pain (2009, background): “TLR4 is also key for microglial activation and the development of pathological pain after peripheral nerve traum”
The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “maintenance phases, following spinal nerve transection (Tanga et al., 2005).”
Pattern recognition receptors in health and diseases (2021, background): “TLR4 exerts its effects through the activation and nuclear localization of NF-κB and the production of pro-inflammatory cytokines, which can activate pain receptors to cause neuropathic pain.(381,382) Relevant studies have revealed for the first time that lysozyme acts as an endogenous ligand for ac”
Microglia-mediated neurotoxicity: uncovering the molecular mechanisms (2007, background): “Independent of LPS, TLR4 also contributes to the initiation of CNS neuroimmune activation and pain neuropathy after transection of the L5 spinal nerv”
Models and mechanisms of hyperalgesia and allodynia. (2009, background): “Intrathecal antisense oligonucleotides directed against the expression of toll-like receptor 4 or knock out of toll-like receptor 4 gene reduces mechanical and thermal hyperalgesia following L5 nerve transection in mice (511).”
Innate immunity and neuroinflammation in the CNS: The role of microglia in Toll‐like receptor‐mediated neuronal injury (2009, background): “For example, both TLR2- and TLR4-deficient mice show decreased expression of proinflammatory genes and decreased pain hypersensitivity after spinal nerve transection (Kim et al., 2007; Tanga et al., 2005).”
p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “The chemokine receptor CCR2 and Toll-like receptor-4 are also expressed in spinal microglia and contribute to neuropathic pain sensitization [27, 28 ].”
Cellular and Molecular Mechanisms of Pain (2009, positive): “Genetic or pharmacological inhibition of TLR2, TLR3, or TLR4 function in mice results not only in decreased microglial activation, but also reduces the hypersensitivity triggered by peripheral nerve injury (Kim et al., 2007; Obata et al., 2008; Tanga et al., 2005).”