Blockade of interleukin-6 signaling inhibits the classic pathway and promotes an alternative pathway of macrophage activation after spinal cord injury in mice
出版年份 2012 全文链接
标题
Blockade of interleukin-6 signaling inhibits the classic pathway and promotes an alternative pathway of macrophage activation after spinal cord injury in mice
作者
关键词
-
出版物
Journal of Neuroinflammation
Volume 9, Issue 1, Pages -
出版商
Springer Nature
发表日期
2012-02-27
DOI
10.1186/1742-2094-9-40
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- Multipotent Adult Progenitor Cells Prevent Macrophage-Mediated Axonal Dieback and Promote Regrowth after Spinal Cord Injury
- (2011) S. A. Busch et al. JOURNAL OF NEUROSCIENCE
- Repertoire of microglial and macrophage responses after spinal cord injury
- (2011) Samuel David et al. NATURE REVIEWS NEUROSCIENCE
- Tumor Necrosis Factor-α Antagonist Reduces Apoptosis of Neurons and Oligodendroglia in Rat Spinal Cord Injury
- (2011) Ke-Bing Chen et al. SPINE
- The LTB4-BLT1 Axis Mediates Neutrophil Infiltration and Secondary Injury in Experimental Spinal Cord Injury
- (2010) Hirokazu Saiwai et al. AMERICAN JOURNAL OF PATHOLOGY
- “Tissue-repairing” blood-derived macrophages are essential for healing of the injured spinal cord: From skin-activated macrophages to infiltrating blood-derived cells?
- (2010) Michal Schwartz BRAIN BEHAVIOR AND IMMUNITY
- Macrophage polarization to a unique phenotype driven by B cells
- (2010) Siew-Cheng Wong et al. EUROPEAN JOURNAL OF IMMUNOLOGY
- Anti-IL-6-receptor antibody promotes repair of spinal cord injury by inducing microglia-dominant inflammation
- (2010) Masahiko Mukaino et al. EXPERIMENTAL NEUROLOGY
- Interferon-γ Decreases Chondroitin Sulfate Proteoglycan Expression and Enhances Hindlimb Function after Spinal Cord Injury in Mice
- (2010) Takayuki Fujiyoshi et al. JOURNAL OF NEUROTRAUMA
- Myelin Activates FAK/Akt/NF-κB Pathways and Provokes CR3-Dependent Inflammatory Response in Murine System
- (2010) Xin Sun et al. PLoS One
- Interferon-γ Produced by Microglia and the Neuropeptide PACAP Have Opposite Effects on the Viability of Neural Progenitor Cells
- (2010) Johanna Mäkelä et al. PLoS One
- Guidance Molecules in Axon Regeneration
- (2010) R. J. Giger et al. Cold Spring Harbor Perspectives in Biology
- Astrocytes initiate inflammation in the injured mouse spinal cord by promoting the entry of neutrophils and inflammatory monocytes in an IL-1 receptor/MyD88-dependent fashion
- (2009) Isabelle Pineau et al. BRAIN BEHAVIOR AND IMMUNITY
- Macrophages and Inflammatory Mediators in Chemical Toxicity: A Battle of Forces
- (2009) Debra L. Laskin CHEMICAL RESEARCH IN TOXICOLOGY
- Overcoming Macrophage-Mediated Axonal Dieback Following CNS Injury
- (2009) S. A. Busch et al. JOURNAL OF NEUROSCIENCE
- Macrophages Promote Axon Regeneration with Concurrent Neurotoxicity
- (2009) J. C. Gensel et al. JOURNAL OF NEUROSCIENCE
- Identification of Two Distinct Macrophage Subsets with Divergent Effects Causing either Neurotoxicity or Regeneration in the Injured Mouse Spinal Cord
- (2009) K. A. Kigerl et al. JOURNAL OF NEUROSCIENCE
- Infiltrating Blood-Derived Macrophages Are Vital Cells Playing an Anti-inflammatory Role in Recovery from Spinal Cord Injury in Mice
- (2009) Ravid Shechter et al. PLOS MEDICINE
- Galectin-3/MAC-2, Ras and PI3K activate complement receptor-3 and scavenger receptor-AI/II mediated myelin phagocytosis in microglia
- (2008) Shlomo Rotshenker et al. GLIA
- Another Barrier to Regeneration in the CNS: Activated Macrophages Induce Extensive Retraction of Dystrophic Axons through Direct Physical Interactions
- (2008) K. P. Horn et al. JOURNAL OF NEUROSCIENCE
- Dynamics of the inflammatory response after murine spinal cord injury revealed by flow cytometry
- (2008) David P. Stirling et al. JOURNAL OF NEUROSCIENCE RESEARCH
Publish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn MoreAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started