The role of the innate immune system in psychiatric disorders
Abstract
There is by now substantial clinical evidence for an association between specific mood disorders and altered immune function. More recently, a number of hypotheses have been forwarded to explain how components of the innate immune system can regulate brain function at the cellular and systems levels and how these may underlie the pathology of disorders such as depression, PTSD and bipolar disorder. In this review we draw reference to biochemical, cellular and animal disease models, as well as clinical observations to elucidate the role of the innate immune system in psychiatric disorders. Proinflammatory cytokines, such as IL-1β IL-6 and TNFα, which feature prominently in the immune response to pathogen in the periphery, have unique and specific actions on neurons and circuits within the central nervous system. Effects of these signaling molecules on neurotransmission, memory, and glucocorticoid function, as well as animal behaviors such as social withdrawal and fear conditioning relevant to psychiatric disorders are elucidated. Finally, we highlight future directions for studies, including the use of peripheral biomarkers, relevant for developing new therapeutic approaches for treating psychiatric illnesses. This article is part of Special Issue entitled 'neuroinflammation in neurodegeneration and neurodysfunction'.
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Inflammation and immune signaling dysregulation can strongly influence neuropsychiatric behavior beyond ASD, with roles in bipolar disorder and PTSD, and perhaps most emphatically in schizophrenia.
“Inflammation and immune signaling dysregulation can strongly influence neuropsychiatric behavior beyond just ASD (Haroon et al, 2012;Meyer and Feldon, 2009), with evidence pointing toward roles in bipolar disorder and PTSD (Jones and Thomsen, 2013), and perhaps most emphatically in schizophrenia (Brown et al, 2004b;Meyer and Feldon, 2009;Michel et al, 2012;Patterson, 2009).”
From The Role of the Immune System in Autism Spectrum Disorder (2017) · cites this paper as Jones and Thomsen, 2013
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- Authors
- Jones, K. A., & Thomsen, C.
- Affiliations
- Lundbeck (United States) (US)
- Corresponding author
- Jones, Kenneth A.
- Venue
- Molecular and Cellular Neuroscience
- Publisher
- Elsevier BV
- Published
- 2013-03
- Volume
- 53
- Pages
- 52-62
- ISSN
- 1044-7431 (ISSN-L)
- OpenAlex
- W1997908175
- Cited by
- 274
- References
- 151
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 12 · 2023: 12 · 2022: 18 · 2021: 21 · 2020: 21 · 2019: 19 · 2018: 20 · 2017: 14 · 2016: 34 · 2015: 26 · 2014: 38 · 2013: 13 · 2012: 3
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular and Cellular Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- innate immune system, neuroinflammation, mental illness, depression, post-traumatic stress disorder, bipolar disorder, inflammatory cytokines, IL-1β, interleukin-6, TNF-α, neurotransmission, memory, glucocorticoid function, social withdrawal, fear conditioning, peripheral biomarkers, animal disease models
- MeSH terms
- Bipolar Disorder, Depressive Disorder, Humans, Immunity, Innate, Stress Disorders, Post-Traumatic, Cytokines
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