Cited by 1,376Immune Response and InflammationMitochondrial Function and PathologyInflammasome and immune disorders

Mitochondria in innate immune responses

Open access
West, A. Phillip, Shadel, Gerald S., Ghosh, Sankar·2011·Nature Reviews Immunology

Abstract

The innate immune system has a key role in the mammalian immune response. Recent research has demonstrated that mitochondria participate in a broad range of innate immune pathways, functioning as signalling platforms and contributing to effector responses. In addition to regulating antiviral signalling, mounting evidence suggests that mitochondria facilitate antibacterial immunity by generating reactive oxygen species and contribute to innate immune activation following cellular damage and stress. Therefore, in addition to their well-appreciated roles in cellular metabolism and programmed cell death, mitochondria appear to function as centrally positioned hubs in the innate immune system. Here, we review the emerging knowledge about the roles of mitochondria in innate immunity.

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nri2975

Cites

103 of 103 references verified0 citation errors · 0 not checkable

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.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Cardiolipin, N-formylated peptides, mtDNA, ATP and reactive oxygen species are known mitochondrial damage-associated molecular patterns.

    “Cardiolipin, N-formylated peptides, mtDNA, ATP and reactive oxygen species are known mitochondrial damage-associated molecular patterns (9, 28–30).”

    From Autoantibodies in Systemic Lupus Erythematosus Target Mitochondrial RNA (2019) · cites this paper as [29]

    The “Mitochondrial DAMPS” section identifies mtDNA and mitochondrial N-formylated peptides as DAMPs. The “Mitochondria and inflammasome activation” section links extracellular ATP and mitochondrial ROS to inflammasome activation, but does not identify either molecule itself as a mitochondrial DAMP; it suggests that intact ATP-producing mitochondria can serve as DAMPs. Cardiolipin was not found in the copy. Page numbers were not available. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Mitochondria and their components, such as N-formylated peptides and mtDNA, are recognized as damage-associated molecular patterns that activate innate immunity and elicit inflammation.

    “Mitochondria and their components (e.g. N-formylated peptides and mtDNA) are recognized as damage-associated molecular patterns (DAMPs), which activate the innate immune system and elicit an inflammatory response6,21–23.”
  • The Nox enzyme family and the respiratory electron transport chain of mitochondria are the two major sources of ROS in many eukaryotic cells.

    “The enzyme family of NADPH oxidases (Nox) [13,83] and the respiratory electron transport chain (ETC) of mitochondria [84,85,86] are the two major sources of ROS in many eukaryotic cells.”

    From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [84]

  • Complex I produces O2− into the mitochondrial matrix where it is dismutated by SOD2 to H2O2.

    “Complex I produces O2●− into the mitochondrial matrix where it is dismutated by SOD2 to H2O2 [67,84,85,86].”

    From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [84]

  • Mitochondria-derived ROS are mainly produced by complexes I and III as O2−.

    “Mitochondria-derived ROS (mtROS) are mainly produced by complexes I and III as O2●−.”

    From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [84]

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

Flagged first, then by citations

Cited by

Sorted by citations

Authors
West, A. P., Shadel, G. S., & Ghosh, S.
Affiliations
  • Yale University (US)
  • Columbia University (US)
Corresponding author
Ghosh, Sankar
Venue
Nature Reviews Immunology
Published
2011-05-20
Volume
11
Issue
6
Pages
389-402
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2033448006
Cited by
1,376
References
103
Citations by year
2026: 119 · 2025: 78 · 2024: 103 · 2023: 97 · 2022: 102 · 2021: 129 · 2020: 101 · 2019: 83 · 2018: 85 · 2017: 109 · 2016: 95 · 2015: 97 · 2014: 75 · 2013: 46 · 2012: 44
FWCI
5.04
Type
journal article
Language
en
Open access
Locations
  • Nature reviews. Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute of Allergy and Infectious Diseases (R37 AI33443, R37AI033443)
  • National Institute of Environmental Health Sciences (ES‑011)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
mitochondria, innate immunity, antiviral signaling, reactive oxygen species, antibacterial immunity, sterile inflammation, programmed cell death, cellular metabolism
MeSH terms
Animals, Bacterial Infections, Humans, Immunity, Innate, Mitochondria, Virus Diseases, Signal Transduction, Reactive Oxygen Species, Models, Immunological, Mitochondrial Proteins

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