Complement Component C1q and Anti‐C1q Antibodies in Theory and in Clinical Practice

Potluková, Eliška; Králíková, Petra

doi:10.1111/j.1365-3083.2008.02089.x

Cited by 65 publications

(66 citation statements)

References 54 publications

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“…1,7 Since C1q must bind to at least two heavy chains in order to change its conformation and activate the classical complement pathway, its activation occurs only after binding to immunoglobulins (Igs) in the form of immune complexes bound to multivalent antigens. 7 The genes encoding for the A, B, and C chains of human Clq are located within the region 1p34.1-1p36.3 on the short arm of chromosome 1. 8 Mutations leading to Clq deficiency have been found in all three chains and are recessive in nature.…”

Section: Introductionmentioning

confidence: 99%

Anti-C1q in systemic lupus erythematosus

Stojan

Petri

2016

Lupus

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C1q is the first component of the classical complement pathway. Both clinically validated inhouse ELISA assays as well as commercial ELISA kits are used for detection of anti-C1q antibodies. Anti-C1q autoantibodies can be detected in a wide range of autoimmune diseases and are highly sensitive for hypocomplementemic uticarial vasculitis. In SLE, anti-C1q are strongly associated with proliferative lupus nephritis, and their absence carries a negative predictive value for development of lupus nephritis of close to 100%. Anti-C1q in combination with anti-dsDNA and low complement has the strongest serological association with renal involvement. The anti-C1q titers correlate with global disease activity scores in patients with renal involvement, and higher titers seem to precede renal flares. After the successful treatment of a renal flare, anti-C1q has the tendency to decrease or even become undetectable. The main obstacle to the inclusion of anti-C1q in the classification criteria and clinical management of SLE is the lack of standardized laboratory assays. Lupus (2016) 25, 873-877.

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Section: Introductionmentioning

confidence: 99%

Anti-C1q in systemic lupus erythematosus

Stojan

Petri

2016

Lupus

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“…Among those autoantibodies, antichromatin/antinucleosome antibodies [Bruns et al 2000;Gomez-Puerta et al 2008;Koutouzov et al 2004], along with anti-C1q antibodies [Pickering and Botto, 2010;Potlukova and Kralikova, 2008] (see the next section), have shown some promise as biomarkers of renal involvement. Chromatin, the DNA-histone complex found in the nucleus of eukaryotic cells, is organized into a repeating series of nucleosomes.…”

Section: Antinucleosome Antibodiesmentioning

confidence: 99%

Biomarkers in systemic lupus erythematosus: challenges and prospects for the future

Liu

Kao

Manzi

et al. 2013

Therapeutic Advances in Musculoskeletal

106

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Abstract:The search for lupus biomarkers to diagnose, monitor, stratify, and predict individual response to therapy is currently more intense than ever before. This effort is essential for several reasons. First, epidemic overdiagnosis and underdiagnosis of lupus, even by certified rheumatologists, leads to errors in therapy with concomitant side effects which may be more serious than the disease itself. Second, identification of lupus flares remains as much an art as it is a science. Third, the capacity to stratify patients so as to predict those who will develop specific patterns of organ involvement is not currently possible but would potentially lead to preventive therapeutic strategies. Fourth, only one new drug for the treatment of lupus has been approved by the US Food and Drug Administration in over 50 years. A major obstacle in this pipeline is the dearth of biomarkers available to prove a patient has responded to an experimental therapeutic intervention. This review will summarize the challenges faced in the discovery and validation of lupus biomarkers, the most promising lupus biomarkers identified to date, and the promise of future directions.

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“…However, although it is likely that they alter the physiological role of C1q, e.g. the uptake of immune complexes and apoptotic debris [17], the pathogenic role of anti-C1q still needs to be elucidated. Independently antiC1q might serve as a biomarker of active lupus nephritis.…”

Section: Introductionmentioning

confidence: 99%

Anti-C1q antibodies as a follow-up marker in SLE patients

Bock

Heijnen

Trendelenburg

2013

Molecular Immunology

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In cross-sectional studies autoantibodies against complement C1q (anti-C1q) were found to be highly associated with active lupus nephritis. The aim of this retrospective study was to determine the value of anti-C1q as follow-up marker of disease activity and renal involvement in patients with systemic lupus erythematosus (SLE). Fifty-two patients with SLE and a minimum of three anti-C1q measurements during follow-up were analyzed. Anti-C1q levels correlated with global disease activity scores. In subgroup analyses, patients without renal involvement did not show a significant correlation between anti-C1q levels and disease activity. In contrast, in patients with renal involvement, anti-C1q levels correlated well with global disease activity. In addition, a positive correlation with the urine protein-tocreatinine ratio and anti-dsDNA antibody levels as well as a negative correlation with complement levels was observed. Anti-C1q antibodies were found to strongly correlate with parameters of SLE disease activity during follow-up, in particular with regard to renal involvement.

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Complement Component C1q and Anti‐C1q Antibodies in Theory and in Clinical Practice

Cited by 65 publications

References 54 publications

Anti-C1q in systemic lupus erythematosus

Anti-C1q in systemic lupus erythematosus

Biomarkers in systemic lupus erythematosus: challenges and prospects for the future

Anti-C1q antibodies as a follow-up marker in SLE patients

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