Autoantibodies against complement component C1q in systemic lupus erythematosus
Open accessAbstract
Systemic lupus erythematosus (SLE) is the archetype of a systemic autoimmune disease, but the multifaceted pathogenic mechanisms leading to inflammation and organ damage are not fully understood. Homozygous deficiency of complement C1q, the first component of the classical pathway of complement, is strongly associated with the development of SLE, thus pointing at a primarily protective role of C1q. However, while most SLE patients do not have hereditary C1q deficiency, there is indirect evidence for the importance of C1q in the inflammatory processes of the disease, including hypocomplementemia as a result of activation via the classical pathway, deposition of C1q in affected tissues and the occurrence of autoantibodies against C1q (anti‐C1q). The growing body of knowledge on anti‐C1q led to the establishment of a biomarker that is used in the routine clinical care of SLE patients. Exploring the binding characteristics of anti‐C1q allows to understand the mechanisms, that lead to the expression of relevant autoantigenic structures and the role of genetic as well as environmental factors. Lastly, the analysis of the pathophysiological consequences of anti‐C1q is of importance because C1q, the target of anti‐C1q, is a highly functional molecule whose downstream effects are altered by the binding of the autoantibody. This review summarises current study data on anti‐C1q and their implications for the understanding of SLE.
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Routine detection of AMA is performed either by indirect immunofluorescence or ELISA.
“Routine detection of AMA is performed either by indirect immunofluorescence or ELISA (48).”
From Identification of Mitofusin 1 and Complement Component 1q Subcomponent Binding Protein as Mitochondrial Targets in Systemic Lupus Erythematosus (2022) · cites this paper as [48]
The Characteristics of anti-C1q section describes an ELISA for detecting anti-C1q antibodies, not AMA. A search for AMA, antimitochondrial antibodies, and indirect immunofluorescence found no passage addressing the claimed routine detection methods. (LLM, conf=0.75)
Experimental — accuracy not yet measured
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Self-citationRenal cell apoptosis in human lupus nephritis: a histological study
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Functional domains of the human C1q A-chain.
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Some Speculations on the Origins of Autoantibodiesa
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- Authors
- Trendelenburg, M.
- Affiliations
- University of Basel (CH)
- Corresponding author
- Trendelenburg, Marten
- Venue
- Clinical & Translational Immunology
- Publisher
- Wiley
- Published
- 2021-01
- Volume
- 10
- Issue
- 4
- Pages
- e1279-e1279
- ISSN
- 2050-0068 (ISSN-L)
- PMC
- PMC8082710
- OpenAlex
- W3158333192
- Cited by
- 48
- References
- 101
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 15 · 2023: 5 · 2022: 10 · 2021: 3
- FWCI
- 1.35
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Clinical & Translational Immunology (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (172965, 310030)
- Idorsia Pharmaceuticals
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Vasculitis and related conditions
- Keywords
- systemic lupus erythematosus, C1q, anti-C1q autoantibodies, C1q deficiency, classical complement pathway, hypocomplementemia, autoantigens, biomarkers, lupus pathogenesis
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