ArticleClinical and experimental immunology2001
Immune complex processing in C1q-deficient mice.
Article in Clinical and experimental immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- A subset of type-II collagen-binding antibodies prevents experimental arthritis by inhibiting FCGR3 signaling in neutrophils.Nature communications · 2023Article
- Engineering of Fc Multimers as a Protein Therapy for Autoimmune Disease.Frontiers in immunology · 2020Review
- Malaria inhibits surface expression of complement receptor 1 in monocytes/macrophages, causing decreased immune complex internalization.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- C1q deficiency leads to the defective suppression of IFN-alpha in response to nucleoprotein containing immune complexes.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Review
- B cells in glomerulonephritis: focus on lupus nephritis.Seminars in immunopathology · 2007Review
- Article
- Both Fcgamma and complement receptors mediate transfer of immune complexes from erythrocytes to human macrophages under physiological flow conditions in vitro.Clinical and experimental immunology · 2006Article
- Monocytosis and accelerated activation of lymphocytes in C1q-deficient autoimmune-prone mice.Immunology · 2004Article
- Dnase1l3 deficiency in lupus-prone MRL and NZB/W F1 mice.Clinical and experimental immunology · 2003Article
- Continual low-level activation of the classical complement pathway.The Journal of experimental medicine · 2001Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Complement and Fcgamma receptors are known to mediate the processing of immune complexes (IC), and abnormalities in these mechanisms may predispose to the development of lupus. We explored the processing of IC in mice deficient in complement component C1q. 125I-labelled IC comprising Hepatitis B surface antigen (HBsAg)/human anti-HBsAg (HBsAg/Ab) were injected intravenously and the sites of IC clearance determined by direct counting of organ uptake at various time points. The liver and spleen were the main sites of IC uptake in all mice. The splenic uptake of IC was significantly reduced in the C1q-deficient mice compared with the control mice. C1q-deficient mice also exhibited an initial accelerated hepatic uptake of IC similar to that seen in human subjects with hypocomplementaemia. The hepatic localization of IC at later time points was similar in both groups of mice. These data in mice are consistent with previous observations in humans that confirm that the classical pathway of complement plays an important role in the appropriate processing of IC in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.