ArticleThe Journal of biological chemistry2015
Macrophage-T cell interactions mediate neuropathic pain through the glucocorticoid-induced tumor necrosis factor ligand system.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 97 citations in OpenAlex.
- A critical role for α7 nicotinic acetylcholine receptor signaling in myeloid lineage cells in chronic neuropathic and inflammatory pain responses.The journal of pain · 2026Article
- Macrophage-induced immunomodulation in oral tissue repair and regeneration: Recent advances and future perspectives.Journal of advanced research · 2026Review
- MAPK-dependent release of GDNF from Schwann cells mediates tumor-independent pain in neurofibromatosis 1.Science signaling · 2026Article
- Glucocorticoid-Induced Tumor Necrosis Factor Receptor Ligand: Correlation and Therapeutic Potential for Cognitive Impairment in Temporal Lobe Epilepsy.Clinical and translational science · 2026Article
- Potential role for immune cell signatures as predictors of acute and chronic pain in adolescents post major musculoskeletal surgery.Brain, behavior, and immunity · 2026Observational
- Inhibition of Macrophage Activation by Minocycline Attenuates CCI-Induced Neuropathic Pain.Inflammation · 2025Article
- Article
- Emerging role of macrophages in neuropathic pain.Journal of orthopaedic translation · 2025Review
- Comprehensive Mechanisms and Non-Invasive Treatment for Complex Regional Pain Syndrome: A Narrative Review.Journal of pain research · 2025Review
- Insights into Vincristine-Induced Peripheral Neuropathy in Aged Rats: Wallerian Degeneration, Oxidative Damage, and Alterations in ATPase Enzymes.ACS chemical neuroscience · 2024Article
- Degenerative and regenerative peripheral processes are associated with persistent painful chemotherapy-induced neuropathies in males and females.Scientific reports · 2024Article
- Discovery of a CCR2-targeting pepducin therapy for chronic pain.Pharmacological research · 2024Article
- Inflammation, Autoimmunity, and Infection in Fibromyalgia: A Narrative Review.International journal of molecular sciences · 2024Review
- T cells at the interface of neuroimmune communication.The Journal of allergy and clinical immunology · 2024Review
- TNF Superfamily and ILC2 Activation in Asthma.Biomolecules · 2024Review
- Review
- Neuroimmune Mechanisms Underlying Post-acute Sequelae of SARS-CoV-2 (PASC) Pain, Predictions from a Ligand-Receptor Interactome.Current rheumatology reports · 2023Review
- Hyaluronic Acid-Based Nanosystems for CD44 Mediated Anti-Inflammatory and Antinociceptive Activity.International journal of molecular sciences · 2023Review
- Pain-resolving immune mechanisms in neuropathic pain.Nature reviews. Neurology · 2023Review
- Mechanisms of Transmission and Processing of Pain: A Narrative Review.International journal of environmental research and public health · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral neuroinflammation caused by activated immune cells can provoke neuropathic pain. Herein, we investigate the actions of macrophages and T cells through glucocorticoid-induced tumor neurosis factor receptor ligand (GITRL) and its receptor (GITR) in neuropathic pain. After partial sciatic nerve ligation (PSL) in enhanced green fluorescent protein (eGFP) chimeric mice generated by the transplantation of eGFP(+) bone marrow cells, eGFP(+) macrophages, and T cells markedly migrated to the injured site after PSL. Administration of agents to deplete macrophages (liposome-clodronate and Clophosome-A(TM)) or T cells (anti-CD4 antibody and FTY720) could suppress PSL-induced thermal hyperalgesia and tactile allodynia. The expression levels of co-stimulatory molecules GITRL and GITR were increased on infiltrating macrophages and T cells, respectively. The perineural injection of a GITRL neutralizing antibody that could inhibit the function of the GITRL-GITR pathway attenuated PSL-induced neuropathic pain. Additionally, the induction of inflammatory cytokines and the accumulation of GITR(+) T cells in the injured SCN were abrogated after macrophage depletion by Clophosome-A(TM). In conclusion, GITRL expressed on macrophages drives cytokine release and T cell activation, resulting in neuropathic pain via GITR-dependent actions. The GITRL-GITR pathway might represent a novel target for the treatment of neuropathic pain.
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