Inflammaging decreases adaptive and innate immune responses in mice and humans
Open accessAbstract
Both the innate and adaptive immune systems decline with age, causing greater susceptibility to infectious diseases and reduced responses to vaccination. Diseases are more severe in elderly than in young individuals and have a greater impact on health outcomes such as morbidity, disability and mortality. Aging is characterized by increased low-grade chronic inflammation, called "inflammaging", measured by circulating levels of TNF-α, IL-6 and CRP, as well as by latent infections with viruses such as cytomegalovirus. Inflammaging has received considerable attention because it proposes a link between changes in immune cells and a number of diseases and syndromes typical of old age. In this review we aim at summarizing the current knowledge on pathways contributing to inflammaging, on immune responses down-regulated by inflammation and mechanisms proposed. The defects in the immune response of elderly individuals presented in this review should help to discover avenues for effective intervention to promote healthy aging.
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?
Multiple factors can contribute to ageing-associated inflammation.
“Multiple factors can contribute to ageing-associated inflammation2; however, the molecular pathways that transduce aberrant inflammatory signalling and their impact in natural ageing remain unclear.”
From cGAS–STING drives ageing-related inflammation and neurodegeneration (2023) · cites this paper as [2]
Longer term treatments (from 20 to 26 months of age) with 3TC were effective at opposing several known phenotypes of aging: macrophage infiltration of tissues, glomerulosclerosis of the kidney and skeletal muscle atrophy.
“Longer term treatments (from 20 to 26 months of age) were effective at opposing several known phenotypes of aging: macrophage infiltration of tissues, a hallmark of chronic inflammation23,25, glomerulosclerosis of the kidney26 and skeletal muscle atrophy27 (Fig. 4e).”
From L1 drives IFN in senescent cells and promotes age-associated inflammation (2019) · cites this paper as [25]
Elevated baseline inflammation may aggravate or cause intrinsic defects in T cells and B cells, hampering their responses to antigenic stimulation.
“It has been suggested that elevated baseline inflammation may aggravate or cause intrinsic defects in T cells and B cells, hampering their responses to antigenic stimulation (summarized in [158]).”
From Aging of the immune system: Focus on inflammation and vaccination (2016) · cites this paper as [158]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 118 · Cited by 357
- Authors
- Frasca, D., & Blomberg, B. B.
- Affiliations
- University of Miami (US)
- Corresponding author
- Frasca, Daniela
- Venue
- Biogerontology
- Published
- 2015-04-29
- Volume
- 17
- Issue
- 1
- Pages
- 7-19
- ISSN
- 1389-5729 (ISSN-L)
- 1573-6768
- PMC
- PMC4626429
- OpenAlex
- W2023503125
- Cited by
- 357
- References
- 118
- Citations by year
- 2026: 21 · 2025: 43 · 2024: 25 · 2023: 32 · 2022: 50 · 2021: 41 · 2020: 28 · 2019: 46 · 2018: 24 · 2017: 22 · 2016: 20 · 2015: 4
- FWCI
- 2.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Biogerontology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG032576, R37AG023717, AG32576, AG042826, R01AG023717, AG 023717, R56AG032576, R21AG042826)
- National Institute of Allergy and Infectious Diseases (R21AI096446, AI096446)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
- Keywords
- inflammaging, aging, innate immunity, adaptive immunity, low-grade inflammation, immunosenescence, vaccine response, infection susceptibility, cytomegalovirus, viral latency, TNF-α, interleukin-6, C-reactive protein, healthy aging
- MeSH terms
- Aging, Animals, Disease Susceptibility, Humans, Immunity, Innate, Inflammation, Species Specificity, Cytokines, Models, Immunological, Inflammation Mediators, Evidence-Based Medicine, Mice, Adaptive Immunity
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
