Cytokine, Sickness Behavior, and Depression
By Robert Dantzer. Immunology and allergy clinics of North America, 2009
1,059 citations recorded by the source corpus.
Summary Sufficient evidence is now available to accept the concept that the brain recognizes cytokines as molecular signals of sickness. Clarifying the way the brain processes information generated by the innate immune system is accompanied by a progressive elucidation of the cellular and molecular components of the intricate system that mediates cytokine-induced sickness behavior. We are still far, however, from understanding the whole. Among the hundreds of genes that proinflammatory cytokines can induce in their cellular targets, only a handful has been examined functionally. In addition, a dynamic view of the cellular interactions that occur at the brain sites of cytokine production and action is missing, together with a clarification of the mechanisms that favor the transition toward pathology.
Subfields: Behavioral Neuroscience, Biological Psychiatry, Neurology
View Paper: https://www.semanticscholar.org/paper/64b39b85545bdacf72507ab067ab782ad44712f3
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In Behavioral Neuroscience
- C. D’Mello
- V. Perry
- J. French
- Neil A. Harrison
- M. Swain
- Marcus A. Gray
- Hugo D. Critchley
- C. Nemeroff
In Biological Psychiatry
- C. Cunningham
- V. Perry
- T. Wyss‐Coray
- C. D’Mello
- J. French
- Neil A. Harrison
- Michael T. Heneka
- M. Swain
In Neurology
- R. Ransohoff
- Beth Stevens
- C. Cunningham
- Marco Prinz
- V. Perry
- Alexei Verkhratsky
- O. Butovsky
- Helmut Kettenmann
Citations in the corpus
- Inflammation Causes Mood Changes Through Alterations in Subgenual Cingulate Activity and Mesolimbic Connectivity (2009, positive): “These changes might underpin the marked reduction in social behavior associated with acute sickness, possibly reflecting an internal self-reorientation of attentional focus (9) and the heterogeneity of symptoms associated with inflammationassociated mood change.”
- The Bidirectional Relationship of Depression and Inflammation: Double Trouble (2020, positive): “IDO is activated in macrophages, dendritic cells, endothelial cells, and brain glial cells comprising microglia (Dantzer, 2009) by signaling from proinflammatory cytokines, such as IL-1β, TNF, and IFN-γ, as well as psychological stress or glucocorticoids (Kiank et al.”
- The role of inflammation in epilepsy (2010, positive): “Chronic activation of cytokine-dependent inflammatory signaling might precipitate the development of depressive behaviors, 155 and could, conceivably, contribute to neuronal dysfunction manifesting as cognitive deficits.”
- Microglia states and nomenclature: A field at its crossroads (2022, positive): “106 This complex and coordinated response, in which the functional role of microglia remains poorly understood, gives rise to adaptive behavioral strategies, including lethargy.”
- Cerebral Microglia Recruit Monocytes into the Brain in Response to Tumor Necrosis Factorα Signaling during Peripheral Organ Inflammation (2009, background): “Interestingly, these three brain areas have been implicated in the regulation of behavior and therefore our current findings could have implications for behavioral changes seen in BDR mice (Dantzer, 2006; Dantzer et al., 2008).”