Microglia: active sensor and versatile effector cells in the normal and pathologic brain
By U. Hanisch, Helmut Kettenmann. Nature Neuroscience, 2007
3,617 citations recorded by the source corpus.
Subfields: Immunology, Neurology, Oncology
View Paper: https://www.semanticscholar.org/paper/ad826b79880c3bdff76ce4addae289ea88ba1e16
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- R. Ransohoff
- B. Barres
- Guo-Yuan Yang
- Yongting Wang
- Jixian Wang
- Yuanyuan Ma
- David J. Loane
- Marco Prinz
In Neurology
- R. Ransohoff
- M. Sofroniew
- B. Barres
- J. Burda
- Alexei Verkhratsky
- David J. Loane
- Beth Stevens
- V. Perry
In Oncology
- R. Yirmiya
- I. Goshen
- M. Sofroniew
- J. Burda
- R. Ransohoff
- Alexei Verkhratsky
- F. Kirchhoff
- Charity E. Onore
Citations in the corpus
- Depression as a microglial disease. (2015, background): “The microglial activation process is controlled by exogenous and endogenous ‘alarm’ molecules (‘on’ signals) or by suppressed production of microglia-inhibitory molecules that are constitutively produced in the brain, usually by neurons (‘off’ signals) [178].”
- Microglial Interactions with Synapses Are Modulated by Visual Experience (2010, background): “. In the event of pathological insult, microglia rapidly become activated, thicken and retract their processes, migrate to the site of injury, proliferate, and participate in the presentation of antigens, phagocytosis of cellular debris, and secretion of proteases that promote microglial motility, a”
- The role of immune dysfunction in the pathophysiology of autism (2011, positive): “Both IL-6 and IL-1b are involved in mediating ‘‘sickness behavior,’’ an adaptive change in behaviors accompanying inflammation that are characterized by lethargy, depression, loss of appetite, anxiety, impaired ability to focus and social withdrawal (Harden et al., 2008).”
- Innate immunity in the central nervous system. (2012, neutral): “PYD, pyrin domain. death or injury removes this suppression (46).”
- Genetic Evidence Implicates the Immune System and Cholesterol Metabolism in the Aetiology of Alzheimer's Disease (2010, background): “However, until now, these observations have been considered to be consequences of disease pathology because activation of microglia, the resident immune cells of the brain, can result from neurodegeneration [39].”
- Microglia/Macrophage Polarization Dynamics Reveal Novel Mechanism of Injury Expansion After Focal Cerebral Ischemia (2012, background): “Microglia/macrophage activation is proposed to benefit the injured brain by removing cell debris and restoring tissue integrity.(12,15) However, mounting evidence reveals that drastic microglia/macrophage activation leads to secondary expansion of ischemic infarction and deterioration of neurologica”
- Selective transfer of exosomes from oligodendrocytes to microglia by macropinocytosis (2011, background): “Induction of a pro-inflammatory reaction can also be induced by serum components, such as immunoglobulin–antigen complexes or opsonising complement (Hanisch and Kettenmann, 2007).”