A calculated response: control of inflammation by the innate immune system
Open accessAbstract
Inflammation is a rapid yet coordinated response that can lead to the destruction of microbes and host tissue. Triggers capable of inducing an inflammatory response include tissue damage and infection by pathogenic and nonpathogenic microbes. Each of these triggers represents a qualitatively distinct stress to the host immune system, yet our understanding of whether they are interpreted as such remains poor. Accumulating evidence suggests that recognition of these distinct stimuli converges on many of the same receptors of the innate immune system. Here I provide an overview of these innate receptors and suggest that the innate immune system can interpret the context of an inflammatory trigger and direct inflammation accordingly.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
When activation of the inflammatory response is altered or prolonged, it can cause more damage to a host than the pathogen itself.
“Recently, however, evidence has accumulated showing that when activation of the inflammatory response is altered or prolonged, it can actually cause more damage to a host than the pathogen itself (Barton, 2008).”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Barton, 2008
These conditions include asthma, rheumatoid arthritis, inflammatory bowel disease, metabolic syndrome, coronary heart disease, and chronic pain.
“These conditions include asthma, rheumatoid arthritis, inflammatory bowel disease, metabolic syndrome, coronary heart disease, and chronic pain”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Barton, 2008
The Introduction and “Perspectives and challenges” sections discuss triggers and regulation of inflammation, but do not identify the six conditions in the claim. Searches for the condition names and for related terms returned no passage connecting this paper to that list; no page numbers were provided in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measuredPatients who have certain somatic and physical disorders with an underlying inflammatory component also have a high likelihood of being or becoming depressed.
“patients who have certain somatic and physical disorders with an underlying inflammatory component also have a high likelihood of being or becoming depressed”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Barton, 2008
The Introduction and Sterile inflammation sections discuss how infection and tissue injury trigger inflammation, but do not address depression in patients with inflammatory disorders. Searches for depression, depressive symptoms, and somatic disorders found no passage supporting the claimed likelihood of being or becoming depressed. No page numbers were available in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThe biological embedding of exaggerated neuro-inflammatory responses to threat is hypothesized to increase a person's risk for depression and possibly other physical and aging-related disorders that have an inflammatory component.
“Ultimately, it is this biological embedding of exaggerated neuro-inflammatory responses to threat that is hypothesized to increase a person's risk for depression and, possibly, other physical and aging-related disorders that have an inflammatory component”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Barton, 2008
The Introduction and 'Degrees of inflammation' discuss innate immune responses to infection and tissue injury, while 'Perspectives and challenges' discusses how those responses are regulated. Searches for biological embedding, neuroinflammatory threat responses, depression, and aging-related disorders found no passage linking these to disease risk. (LLM, conf=0.76)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Neutrophils and immunity: challenges and opportunities
Nathan, C. (2006) · Nature reviews. Immunology · doi:10.1038/nri1785 · Cited by 2,971 · see citing works
Resolution of inflammation: the beginning programs the end
Serhan, C. N., & Savill, J. (2005) · Nature Immunology · doi:10.1038/ni1276 · Cited by 2,552 · see citing works
Innate Immunity: The Virtues of a Nonclonal System of Recognition
Medzhitov, R., & Janeway, C. A. (1997) · Cell · doi:10.1016/s0092-8674(00)80412-2 · Cited by 2,434 · see citing works
Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide
Lande, R., Gregorio, J., Facchinetti, V., Chatterjee, B., Wang, Y.-H., Homey, B., Cao, W., Wang, Y.-H., Su, B., Nestle, F. O., et al. (2007) · Nature · doi:10.1038/nature06116 · Cited by 1,910 · see citing works
Innate immune recognition of viral infection
Kawai, T., & Akira, S. (2006) · Nature Immunology · doi:10.1038/ni1303 · Cited by 1,899 · see citing works
Nathan, C., & Shiloh, M. U. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.97.16.8841 · Cited by 1,469 · see citing works
Lipid mediator class switching during acute inflammation: signals in resolution
Levy, B. D., Clish, C. B., Schmidt, B., Gronert, K., & Serhan, C. N. (2001) · Nature Immunology · doi:10.1038/89759 · Cited by 1,453 · see citing works
Chen, C.-J., Kono, H., Golenbock, D., Reed, G., Akira, S., & Rock, K. L. (2007) · Nature Medicine · doi:10.1038/nm1603 · Cited by 876 · see citing works
Flagged first, then by citations
Research works printed but not linked: 2
- Kumar, V., Abbas, A.K., Fausto, N., and Mitchell, M. 2007. Robbins basic pathology. W.B. Saunders. Philadelphia, Pennsylvania, USA. 960 pp.
- O'Riordan, M., Yi, C.H., Gonzales, R., Lee, K.D., and Portnoy, D.A. 2002. Innate recognition of bacteria by a macrophage cytosolic surveillance pathway. Proc. Natl. Acad. Sci. U. S. A. 99:13861-13866.
Cited by
Sorted by citations
Origin and physiological roles of inflammation
Medzhitov, R. (2008) · Nature · doi:10.1038/nature07201 · Cited by 6,618 · see citing works
Slavich, G. M., & Irwin, M. R. (2014) · Psychological Bulletin · doi:10.1037/a0035302 · Cited by 2,206 · see citing works
Gut microbiota–brain axis in depression: the role of neuroinflammation
Carlessi, A. S., Borba, L. A., Zugno, A. I., Quevedo, J., & Réus, G. Z. (2021) · European Journal of Neuroscience · doi:10.1111/ejn.14631 · Cited by 243 · see citing works
Qureshi, R., Picon-Ruiz, M., Aurrekoetxea-Rodriguez, I., Nunes de Paiva, V., D’Amico, M., Yoon, H., Radhakrishnan, R., Morata-Tarifa, C., Ince, T., Lippman, M. E., et al. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2020.05.008 · Cited by 127 · see citing works
Ray, A., Chakraborty, K., & Ray, P. (2013) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2013.00052 · Cited by 108 · see citing works
Maatouk, L., Compagnion, A.-C., Sauvage, M.-A. C.-D., Bemelmans, A.-P., Leclere-Turbant, S., Cirotteau, V., Tohme, M., Beke, A., Trichet, M., Bazin, V., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-04569-y · Cited by 95 · see citing works
Popescu, M., Cabrera-Martinez, B., & Winslow, G. M. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1900484 · Cited by 72 · see citing works
Williams, J., Sergi, D., McKune, A. J., Georgousopoulou, E. N., Mellor, D. D., & Naumovski, N. (2019) · Phytotherapy Research · doi:10.1002/ptr.6277 · Cited by 73 · see citing works
ten Brink, T., Damanik, F., Rotmans, J. I., & Moroni, L. (2024) · Advanced Healthcare Materials · doi:10.1002/adhm.202301939 · Cited by 71 · see citing works
Bilal, M., Ashraf, S., & Zhao, X. (2022) · Frontiers in Nutrition · doi:10.3389/fnut.2022.931458 · Cited by 58 · see citing works
l-Theanine as a Functional Food Additive: Its Role in Disease Prevention and Health Promotion
Williams, J., Kellett, J., Roach, P., McKune, A., Mellor, D., Thomas, J., & Naumovski, N. (2016) · Beverages · doi:10.3390/beverages2020013 · Cited by 52 · see citing works
- Authors
- Barton, G. M.
- Affiliations
- University of California, Berkeley (US)
- Corresponding author
- Barton, Gregory M.
- ORCID
- Barton, Gregory M.
- Venue
- Journal of Clinical Investigation
- Published
- 2008-02-01
- Volume
- 118
- Issue
- 2
- Pages
- 413-420
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC2214713
- OpenAlex
- W2053411326
- Cited by
- 532
- References
- 8
- Citations by year
- 2026: 18 · 2025: 25 · 2024: 24 · 2023: 29 · 2022: 35 · 2021: 29 · 2020: 29 · 2019: 38 · 2018: 27 · 2017: 27 · 2016: 29 · 2015: 25 · 2014: 38 · 2013: 28 · 2012: 31
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- UC Berkeley College of Chemistry
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- inflammation, innate immunity, innate immune receptors, pattern recognition receptors, tissue damage, infection, host-pathogen interaction
- MeSH terms
- Animals, Humans, Immunity, Innate, Infections, Inflammation, Receptors, Pattern Recognition
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
