A Mitochondrial Checkpoint in Autoimmune Disease
Open accessAbstract
Cell-fate decisions in innate and adaptive immune cells are metabolically regulated and modified by tissue-derived signals, thereby balancing protective and pathogenic immunity. Reporting in Science, Ling et al. (2018) have identified C1q as a mitochondrial activator that suppresses exuberant anti-self and anti-viral CD8 T cell effector responses to prevent autoimmune disease.
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Confocal microscopy analyses indicate that C1q and C1qBP co-localize in mitochondria.
“confocal microscopy analyses indicate that C1q and C1qBP co-localized in mitochondria”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [83]
The passage labeled Abstract (page unavailable) says that C1q bound to its receptor p32 and translocated to mitochondria, supporting an association there. It does not identify p32 as C1qBP or report confocal microscopy showing co-localization, so the specific imaging claim is not established by this copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredTogether these findings suggest that C1q regulates mitochondrial activity in memory precursor effector cells and that impairment of this regulation leads to expansion of autoreactive pro-inflammatory short-lived effector cells and suppression of protective memory precursor effector cells.
“Together, these elements suggest that C1q regulates mitochondrial activity in memory precursor effector cells and that an impairment of this regulation leads to an expansion of autoreactive and pro-inflammatory short-lived effector cells and the suppression of protective memory precursor effector cells81,83”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [83]
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Cites
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Self-citationC1q restrains autoimmunity and viral infection by regulating CD8 <sup>+</sup> T cell metabolism
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- Authors
- Weyand, C. M., & Goronzy, J. J.
- Affiliations
- VA Palo Alto Health Care System (US)
- Corresponding author
- Weyand, Cornelia M.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2018-08
- Volume
- 28
- Issue
- 2
- Pages
- 185-186
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC6487495
- OpenAlex
- W2885931904
- Cited by
- 12
- References
- 10
- Citations by year
- 2025: 2 · 2024: 1 · 2022: 4 · 2021: 1 · 2020: 3 · 2019: 1
- FWCI
- 0.54
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (R01AR042527, R01HL117913, R01AI108906, P01HL129941, R01AI108891, R01AG045779, U19AI057266, R01AI129191)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- C1q, autoimmune disease, CD8+ T cells, T cell metabolism, antiviral immunity, effector T cell responses, innate immunity, adaptive immunity
- MeSH terms
- Immunity, T-Lymphocytes, Autoimmunity, Complement C1q, CD8-Positive T-Lymphocytes
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