Journal
NATURE REVIEWS IMMUNOLOGY
Volume 16, Issue 1, Pages 22-34Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nri.2015.5
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Funding
- NCATS NIH HHS [UL1 TR000454, UL1 TR002378] Funding Source: Medline
- NCI NIH HHS [P30 CA138292] Funding Source: Medline
- NCRR NIH HHS [UL1 RR025008] Funding Source: Medline
- NHLBI NIH HHS [R01 HL073921] Funding Source: Medline
- NIMH NIH HHS [R21 MH106904, R01 MH067990, R01 MH109637, R01 MH075102, R01 MH083746, R21 MH105897, R03 MH100273, R01 MH060723, R01 MH087604, K05 MH069124, R21 MH077172] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P30CA138292] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR ADVANCING TRANSLATIONAL SCIENCES [UL1TR000454] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [UL1RR025008] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [R21MH077172, R01MH087604, R03MH100273] Funding Source: NIH RePORTER
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Crosstalk between inflammatory pathways and neurocircuits in the brain can lead to behavioural responses, such as avoidance and alarm, that are likely to have provided early humans with an evolutionary advantage in their interactions with pathogens and predators. However, in modern times, such interactions between inflammation and the brain appear to drive the development of depression and may contribute to non-responsiveness to current antidepressant therapies. Recent data have elucidated the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression. Here, we detail our current understanding of these pathways and discuss the therapeutic potential of targeting the immune system to treat depression.
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