ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Peripheral role of cathepsin S in Th1 cell-dependent transition of nerve injury-induced acute pain to a chronic pain state.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 62 citations in OpenAlex.
- The Integrated Transcriptome Bioinformatics Analysis of Energy Metabolism-Related Profiles for Dorsal Root Ganglion of Neuropathic Pain.Molecular neurobiology · 2025Article
- Atopic dermatitis in early life and pain at 10 years of age: An exploratory study.European journal of pediatrics · 2024Article
- TSLP in DRG neurons causes the development of neuropathic pain through T cells.Journal of neuroinflammation · 2023Article
- Identification and validation of biomarkers related to Th1 cell infiltration in neuropathic pain.Journal of inflammation (London, England) · 2023Article
- Decreased PPARgamma in the trigeminal spinal subnucleus caudalis due to neonatal injury contributes to incision-induced mechanical allodynia in female rats.Scientific reports · 2022Article
- Mucosal immunology of the ocular surface.Mucosal immunology · 2022Review
- Role of cathepsin K in the expression of mechanical hypersensitivity following intra-plantar inflammation.Scientific reports · 2022Article
- Differential Expression and Distinct Roles of Proteinase-Activated Receptor 2 in Microglia and Neurons in Neonatal Mouse Brain After Hypoxia-Ischemic Injury.Molecular neurobiology · 2022Article
- Regenerative Role of T Cells in Nerve Repair and Functional Recovery.Frontiers in immunology · 2022Review
- Characteristics, mechanism, and management of pain in atopic dermatitis: A literature review.Clinical and translational allergy · 2021Review
- [Neuropathic pruritus].Schmerz (Berlin, Germany) · 2020Article
- Cathepsin S as a potential therapeutic target for chronic pain.Medicine in drug discovery · 2020Article
- MHCII-restricted T helper cells: an emerging trigger for chronic tactile allodynia after nerve injuries.Journal of neuroinflammation · 2020Review
- Involvement of Cathepsins in Innate and Adaptive Immune Responses in Periodontitis.Evidence-based complementary and alternative medicine : eCAM · 2020Review
- Inhibition of Cathepsin S Reduces Lacrimal Gland Inflammation and Increases Tear Flow in a Mouse Model of Sjögren's Syndrome.Scientific reports · 2019Article
- Corneal pain and experimental model development.Progress in retinal and eye research · 2019Review
- Itch Processing in the Skin.Frontiers in medicine · 2019Review
- [New findings regarding the neurobiology of pruritus].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2018Review
- Analgesic Effect of Methane Rich Saline in a Rat Model of Chronic Inflammatory Pain.Neurochemical research · 2018Article
- CD4+ αβ T cell infiltration into the leptomeninges of lumbar dorsal roots contributes to the transition from acute to chronic mechanical allodynia after adult rat tibial nerve injuries.Journal of neuroinflammation · 2018Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is increasing evidence that CD4(+) T-cell-dependent responses are associated with the maintenance of neuropathic pain. However, little is known about the precise mechanism(s) underlying the activation of CD4(+) T-cells. We herein show that inhibition of cathepsin S (CatS) activity, either through genetic deletion or via a pharmacological inhibitor, Z-Phe-Leu-COCHO (Z-FL), significantly attenuated the maintenance of tactile allodynia, splenic hypertrophy, increased number of splenic CD4(+) T-cells and the final cleavage step of the MHC class II-associated invariant chain following peripheral nerve injury. It was also noted that splenectomy significantly attenuated the peripheral nerve injury-induced tactile allodynia, whereas the adoptive transfer of splenic CD4(+) T-cells from neuropathic wild-type mice significantly increased the pain level of splenectomized wild-type or CatS(-/-) mice. Furthermore, CatS deficiency or Z-FL treatment also significantly inhibited the infiltration of CD4(+) T-cells that expressed interferon-γ (IFN-γ) in the dorsal spinal cord. Signal transducer and activator of transcription 1, a molecule downstream of IFN-γ receptor activation, was activated exclusively in microglia 7 d after peripheral nerve injury. Moreover, CatS deficiency, Z-FL treatment, or splenectomy significantly attenuated the proliferation of microglia 14 d after peripheral nerve injury. These results show a peripheral pivotal role of CatS in the development of neuropathic pain through the antigen-specific activation of CD4(+) T-cells. After activation, CD4(+) T-cells infiltrate into the dorsal spinal cord and secrete IFN-γ to reactivate microglia, which contribute to the transition of acute pain to a chronic pain state.
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