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Critical Reviews™ in Immunology

Publication de 6  numéros par an

ISSN Imprimer: 1040-8401

ISSN En ligne: 2162-6472

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.3 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.6 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00079 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

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Opportunities for Translation from the Bench: Therapeutic Intervention of the JAK/STAT Pathway in Neuroinflammatory Diseases

Volume 35, Numéro 6, 2015, pp. 505-527
DOI: 10.1615/CritRevImmunol.2016015517
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RÉSUMÉ

Pathogenic CD4+ T cells and myeloid cells play critical roles in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS. These immune cells secrete aberrantly high levels of pro-inflammatory cytokines that pathogenically bridge the innate and adaptive immune systems and damage neurons and oligodendrocytes. These cytokines include interleukin-2 (IL-2), IL-6, IL-12, IL-21, IL-23, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon-γ (IFN-γ). It is, therefore, not surprising that both the dysregulated expression of these cytokines and the subsequent activation of their downstream signaling cascades is a common feature in MS/EAE. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is utilized by numerous cytokines for signal transduction and is essential for the development and regulation of immune responses. Unbridled activation of the JAK/STAT pathway by pro-inflammatory cytokines has been demonstrated to be critically involved in the pathogenesis of MS/EAE. In this review, we discuss recent advancements in our understanding of the involvement of the JAK/STAT signaling pathway in the pathogenesis of MS/EAE, with a particular focus on therapeutic approaches to target the JAK/STAT pathway.

CITÉ PAR
  1. Malemud Charles J., Defective JAK-STAT Pathway Signaling Contributes to Autoimmune Diseases, Current Pharmacology Reports, 4, 5, 2018. Crossref

  2. Nabavi Seyed Mohammad, Ahmed Touqeer, Nawaz Maheen, Devi Kasi Pandima, Balan Devasahayam Jaya, Pittalà Valeria, Argüelles-Castilla Sandro, Testai Lara, Khan Haroon, Sureda Antoni, de Oliveira Marcos Roberto, Vacca Rosa Anna, Xu Suowen, Yousefi Bahman, Curti Valeria, Daglia Maria, Sobarzo-Sánchez Eduardo, Filosa Rosanna, Nabavi Seyed Fazel, Majidinia Maryam, Dehpour Ahmad Reza, Shirooie Samira, Targeting STATs in neuroinflammation: The road less traveled!, Pharmacological Research, 141, 2019. Crossref

  3. von Essen Marina, Søndergaard Helle, Petersen Eva, Sellebjerg Finn, IL-6, IL-12, and IL-23 STAT-Pathway Genetic Risk and Responsiveness of Lymphocytes in Patients with Multiple Sclerosis, Cells, 8, 3, 2019. Crossref

  4. Karateev A. E., Nasonov E. L., Chronic pain and central sensitization in immuno-inflammatory rheumatic diseases: pathogenesis, clinical manifestations, the possibility of using targeted disease modifying antirheumatic drugs, Rheumatology Science and Practice, 57, 2, 2019. Crossref

  5. Luo Deling, Fu Jin, Identifying characteristic miRNAs-genes and risk pathways of multiple sclerosis based on bioinformatics analysis, Oncotarget, 9, 4, 2018. Crossref

  6. Xin Ping, Xu Xiaoyun, Deng Chengjie, Liu Shuang, Wang Youzhi, Zhou Xuegang, Ma Hongxing, Wei Donghua, Sun Shiqin, The role of JAK/STAT signaling pathway and its inhibitors in diseases, International Immunopharmacology, 80, 2020. Crossref

  7. Vaes Josine E. G., Brandt Myrna J. V., Wanders Nikki, Benders Manon J. N. L., Theije Caroline G. M., Gressens Pierre, Nijboer Cora H., The impact of trophic and immunomodulatory factors on oligodendrocyte maturation: Potential treatments for encephalopathy of prematurity, Glia, 69, 6, 2021. Crossref

  8. Günaydın Caner, Önger M. Emin, Avcı Bahattin, Bozkurt Ayhan, Terzi Murat, Bilge S. Sırrı, Tofacitinib enhances remyelination and improves myelin integrity in cuprizone-induced mice, Immunopharmacology and Immunotoxicology, 43, 6, 2021. Crossref

  9. Horiuchi Hiroshi, Parajuli Bijay, Komiya Hiroyasu, Ogawa Yuki, Jin Shijie, Takahashi Keita, Azuma Yasu-Taka, Tanaka Fumiaki, Suzumura Akio, Takeuchi Hideyuki, Interleukin-19 Abrogates Experimental Autoimmune Encephalomyelitis by Attenuating Antigen-Presenting Cell Activation, Frontiers in Immunology, 12, 2021. Crossref

  10. Jain Mayank, Singh Mukul Kumar, Shyam Hari, Mishra Archana, Kumar Shailendra, Kumar Ambrish, Kushwaha Jitendra, Role of JAK/STAT in the Neuroinflammation and its Association with Neurological Disorders, Annals of Neurosciences, 28, 3-4, 2021. Crossref

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