ArticleImmunology2004
Monocytosis and accelerated activation of lymphocytes in C1q-deficient autoimmune-prone mice.
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- KCC2 inhibition and neuronal hyperexcitability promote extrinsic apoptosis dependent upon C1q.Frontiers in molecular neuroscience · 2025Article
- Anti-C1q autoantibodies from systemic lupus erythematosus patients enhance CD40-CD154-mediated inflammation in peripheral blood mononuclear cellsClinical & translational immunology · 2022Article
- Emerging and Novel Functions of Complement Protein C1q.Frontiers in immunology · 2015Review
- Genetic variants in the region of the C1q genes are associated with rheumatoid arthritis.Clinical and experimental immunology · 2013Article
- A lupus-susceptibility C57BL/6 locus on chromosome 3 (Sle18) contributes to autoantibody production in 129 mice.Genes and immunity · 2009Article
- Deficiency in complement C1q improves histological and functional locomotor outcome after spinal cord injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Genetic and Molecular Basis of QTL of Diabetes in Mouse: Genes and Polymorphisms.Current genomics · 2008Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
C1q deficiency has been shown to accelerate spontaneous autoimmunity in mice. We studied the time course of activation of monocytes and lymphocytes in autoimmune and non-autoimmune mice in the presence or absence of C1q as a disease accelerator. Autoimmune MRL\Mp.C1qa-\- and non-autoimmune C57BL\6.C1qa-\- mice were analysed at various time points between 6 and 33 weeks of age and compared to strain- and age-matched C1q-sufficient controls. Splenic and peritoneal leucocytes were analysed by flow cytometry and plasma levels of immunoglobulin M (IgM), total IgG, IgG subclasses and IgM autoantibodies were measured. Both C1q-deficient strains had significantly more splenic monocytes than their controls at all time points analysed. In addition, MRL\Mp.C1qa-\- but not C57BL/6.C1qa-\- mice developed splenic hypercellularity starting at about 12-17 weeks old, had signs of accelerated CD4+ T-cell activation and showed a marked increase in splenic plasma cells and total serum IgM levels from about 22 weeks of age. The accelerated CD4+ T-cell activation was not due to a direct inhibitory effect of C1q on T cells. These data show that C1q deficiency causes splenic monocytosis together with accelerated T-cell activation in an autoimmune-prone mouse strain.
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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.