ArticleActa pharmaceutica Sinica. B2023
JAK inhibition ameliorated experimental autoimmune encephalomyelitis by blocking GM-CSF-driven inflammatory signature of monocytes.
Article in Acta pharmaceutica Sinica. B, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
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- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Blood cytokine levels in anti-NMDAR and viral encephalitis during the early stage of hospitalization: a small-sample exploratory pilot study.Frontiers in immunology · 2026Article
- Sp3 ameliorated experimental autoimmune encephalomyelitis by triggering Socs3 in Th17 cells.Journal of advanced research · 2025Article
- Network Pharmacology-Based and Experimental Validation Elucidate the Target Mechanism of Vinorine in Ameliorating Secondary Brain Injury After Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2025Article
- Blurred by a "Puff of Smoke"-A Case-Based Review on the Challenging Recognition of Coexisting CNS Demyelinating Disease and Moyamoya Angiopathy.International journal of molecular sciences · 2025Review
- Beyond cancer: The potential application of CD47-based therapy in non-cancer diseases.Acta pharmaceutica Sinica. B · 2025Review
- Clinical updates of JAK inhibitors in cutaneous granulomatous diseases.Frontiers in immunology · 2025Review
- Harnessing monocyte dynamics for treatment of multiple sclerosis; insights from experimental model studies.Immunotherapy advances · 2025Review
- circWWC3 enhances the progression of triple-negative breast cancer by interacting with vimentin to regulate the secretion of CSF2.Frontiers in immunology · 2025Article
- Emerging interleukin-1 receptor-associated kinase 4 (IRAK4) inhibitors or degraders as therapeutic agents for autoimmune diseases and cancer.Acta pharmaceutica Sinica. B · 2024Review
- Advanced progress in the genetic modification of the oncolytic HSV-1 virus.Frontiers in oncology · 2024Review
- Immunological dimensions of neuroinflammation and microglial activation: exploring innovative immunomodulatory approaches to mitigate neuroinflammatory progression.Frontiers in immunology · 2023Review
- Machine learning and single-cell RNA sequencing analyses identify MS-related monocytes and a five-gene candidate biomarker signature.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocytes are key effectors in autoimmunity-related diseases in the central nervous system (CNS) due to the critical roles of these cells in the production of proinflammatory cytokines, differentiation of T-helper (Th) cells, and antigen presentation. The JAK-STAT signaling is crucial for initiating monocytes induced immune responses by relaying cytokines signaling. However, the role of this pathway in modulating the communication between monocytes and Th cells in the pathogenesis of multiple sclerosis (MS) is unclear. Here, we show that the JAK1/2/3 and STAT1/3/5/6 subtypes involved in the demyelination mediated by the differentiation of pathological Th1 and Th17 and the CNS-infiltrating inflammatory monocytes in experimental autoimmune encephalomyelitis (EAE), a model for MS. JAK inhibition prevented the CNS-infiltrating CCR2-dependent Ly6C
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