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Two Distinct Immune Pathways Linking Social Relationships With Health: Inflammatory and Antiviral Processes
Open accessAbstract
Objective: Social relationships can both influence and be influenced by immune processes. Past work implicates two distinct pathways along which this interaction may occur: inflammatory processes and antiviral processes. This article reviews how social behavior is modulated by these two immune processes and how such processes may in turn regulate social behavior. Methods: This narrative review outlines existing work on social behavior and both inflammatory and antiviral processes. We propose an evolutionary framework that aims to integrate these findings. Specifically, social isolation has evolutionarily increased the likelihood of wounding and therefore increased the need for inflammation, which works to promote healing. Conversely, broader social networks provide protection from physical threats but also lead to increased pathogen exposure, necessitating a more robust antiviral response. Results: This review highlights that social adversity, such as social exclusion or loneliness, is associated with increased inflammation, whereas social contact is associated with increased antiviral immunity. Furthermore, increased inflammation leads to sensitivity to social stimuli, presumably to avoid hostile conspecifics and approach allies who may provide care while vulnerable. Individuals with inadequate antiviral immunity engage in behaviors that minimize pathogen exposure, such as reduced affiliative behavior. Conclusions: This review suggests that adverse social experiences (social isolation, perceived social threat) may induce inflammatory responses while suppressing antiviral immunity, whereas positive experiences of social connection may reduce inflammation and bolster antiviral responses. Although acutely elevated inflammation would be adaptive under conditions where wounding is likely, chronic inflammation related to continued social adversity may have detrimental health consequences.
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Loneliness impairs inflammatory and immune responses and promotes a phenotypic hypersensitivity to social threats and self-centered behavior.
“loneliness impairs inflammatory and immune responses[ 6 , 10 ] and promotes a phenotypic hypersensitivity to social threats and self‐centered behavior.[ 8 , 11 ]”
From Loneliness and the Social Brain: How Perceived Social Isolation Impairs Human Interactions (2021) · cites this paper as [10]
The citation placement points to the claim about inflammatory and immune responses, not the separately cited claim about self-centered behavior. In “Subjective Measures of Social Integration,” the paper links loneliness to reduced antiviral gene expression and poorer vaccine antibody responses. But “Feelings and Perceptions Related to Social Isolation” reports heightened, rather than impaired, inflammatory responses associated with loneliness. (LLM, conf=0.86)
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Loneliness and the Social Brain: How Perceived Social Isolation Impairs Human Interactions
Lieberz, J., Shamay‐Tsoory, S. G., Saporta, N., Esser, T., Kuskova, E., Stoffel‐Wagner, B., Hurlemann, R., & Scheele, D. (2021) · Advanced Science · doi:10.1002/advs.202102076 · Cited by 116
Salazar, S. M. D. C., Dino, M. J. S., & Macindo, J. R. B. (2023) · Journal of Clinical Nursing · doi:10.1111/jocn.16675 · Cited by 11
Metadata
- Authors
- Leschak, C. J., & Eisenberger, N. I.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Eisenberger, Naomi I.
- Venue
- Psychosomatic Medicine
- Published
- 2019-02-14
- Volume
- 81
- Issue
- 8
- Pages
- 711-719
- ISSN
- 0033-3174 (ISSN-L)
- 1534-7796
- PMC
- PMC7025456
- OpenAlex
- W2920250253
- Cited by
- 129
- References
- 32
- Citations by year
- 2026: 11 · 2025: 23 · 2024: 22 · 2023: 21 · 2022: 20 · 2021: 22 · 2020: 9 · 2019: 1
- FWCI
- 8.06
- Type
- journal article
- Language
- en
- Open access
- green
- escholarship.org
- Locations
- Psychosomatic Medicine (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health (HHSN261200800001C)
- National Cancer Institute (HHSN261200800001E))
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32HD091059)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Social Sciences › Health › Health disparities and outcomes
- Keywords
- interpersonal relationships, inflammation, antiviral immunity, social isolation, loneliness, social exclusion, social adversity, social connectedness, evolutionary framework, pathogen exposure, affiliative behavior, social behavior, chronic inflammation
- MeSH terms
- Chronic Disease, Disease Susceptibility, Emotions, Biological Evolution, Humans, Inflammation, Interpersonal Relations, Selection, Genetic, Social Behavior, Psychological Distance, Social Isolation, Social Perception, Virus Diseases, Wounds and Injuries, Neuroimmunomodulation, Models, Immunological, Disease Transmission, Infectious, Feedback, Physiological, Illness Behavior, Social Determinants of Health
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