C1q restrains autoimmunity and viral infection by regulating CD8 + T cell metabolism
Open accessAbstract
Complement is a CD8 + T cell metabolic rheostat: Systemic lupus erythematosus (SLE) is associated with deficiencies in the complement protein C1q. Although C1q plays a role in the clearance of apoptotic cells, there are several redundant clearance pathways. Disruption of one pathway does not lead to an autoimmune defect. In a chronic graft-versus-host disease model of SLE, Ling et al. show that C1q dampens CD8 + T cell responses to self-antigens. C1q modulates metabolism through the mitochondrial cell-surface protein p32/gC1qR. The lack of C1q during a viral infection also enhances CD8 + T cell responses. Thus, C1q plays a role as a “metabolic rheostat” for effector CD8 + T cells. Science , this issue p. 558
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An increase in spare respiratory capacity in CD8+ T cells is a marker of longevity, suggesting that C1q regulates the viability and turnover of memory precursor effector cells.
“An increase in spare respiratory capacity in CD8+ T cells is a marker of longevity, suggesting that C1q regulates the viability and turnover of memory precursor effector”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [81]
The passages on MPECs (page not provided) report impaired spare respiratory capacity in C1q-deficient cells, alongside faster turnover and findings suggesting that C1q influences their viability. Our copy says spare respiratory capacity correlates with mitochondrial mass, but does not identify increased capacity as a marker of CD8+ T-cell longevity. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn mice, C1qBP expression is higher in effector CD8+ T cells than in naive cells.
“In mice, the expression of C1qBP is higher in effector CD8+ T cells than in naive cells”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [81]
The passage discussing Fig. S11B–C reports increased p32/gC1qR expression on activated mouse CD8+ T cells. It does not explicitly compare effector CD8+ T cells with naïve cells, so the claim is more specific than the reported finding. (LLM, conf=0.78)
Experimental — accuracy not yet measuredC1q-deficient mice have increased short-lived effector cells and decreased memory precursor effector cells compared with wild-type littermates, suggesting that C1q promotes survival of short-lived effector cells.
“C1q-deficient mice have increased numbers of short-lived effector cells and decreased numbers of memory precursor effector cells compared with their wild type littermates, suggesting that C1q promotes the survival of short-lived effector cells”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [81]
The passage describing the cGvHD model (indexed as Abstract; page unavailable) reports a relative expansion of short-lived effector cells and a corresponding reduction in memory precursor effector cells in C1q-deficient mice, but gives proportions rather than the absolute numbers claimed. A later passage says C1q controls the survival of memory precursor effector cells, not short-lived effector cells. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn a chronic graft-versus-host-disease model of SLE, C1q but not C3 can modulate mitochondrial metabolism in CD8+ T cells to limit self-reactive responses.
“Investigations of C1q or C3 deficiency in a chronic graft-versus-host-disease model of SLE indicate that C1q, but not C3, could modulate mitochondrial metabolism in CD8+ T cells to limit self-reactive responses81”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [81]
Together 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 [81]
Short-lived effector cells expanded in the absence of C1q contribute to self-reactive responses and tissue inflammation.
“short-lived effector cells, expanded in the absence of C1q, contribute to self-reactive responses and tissue inflammation”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [81]
Mitochondrial spare respiratory capacity and mitochondrial biogenesis are impaired in C1q-deficient memory precursor effector cells.
“The mitochondrial spare respiratory capacity and mitochondrial biogenesis were impaired in C1q-deficient memory precursor effector cells”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [81]
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 [81]
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References 39 · Cited by 199
- Authors
- Ling, G. S., Crawford, G., Buang, N., Bartok, I., Tian, K., Thielens, N. M., Bally, I., Harker, J. A., Ashton-Rickardt, P. G., Rutschmann, S., Strid, J., & Botto, M.
- Affiliations
- Imperial College London (GB)
- Centre National de la Recherche Scientifique (FR)
- Faculty of Medicine, Imperial College London, London W12 ONN, UK.
- Corresponding author
- Botto, Marina
- ORCID
- Venue
- Science
- Published
- 2018-05-04
- Volume
- 360
- Issue
- 6388
- Pages
- 558-563
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC6545171
- OpenAlex
- W2801418288
- Cited by
- 199
- References
- 39
- Citations by year
- 2026: 12 · 2025: 24 · 2024: 31 · 2023: 21 · 2022: 26 · 2021: 25 · 2020: 25 · 2019: 28 · 2018: 7
- FWCI
- 9.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Funders
- Wellcome Trust (108008/Z/15/Z)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- C1q, complement system, systemic lupus erythematosus, autoimmunity, viral infection, efferocytosis, graft-versus-host disease, effector T cells
- MeSH terms
- Animals, Autoantibodies, Complement Pathway, Classical, Complement C3, Disease Models, Animal, Immunoglobulins, Immunologic Memory, Lupus Erythematosus, Systemic, Lymphocytic Choriomeningitis, Mice, Mutant Strains, Autoimmunity, Complement C1q, CD8-Positive T-Lymphocytes, Mice
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