ArticleThe Journal of experimental medicine2003
The B cell receptor itself can activate complement to provide the complement receptor 1/2 ligand required to enhance B cell immune responses in vivo.
Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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.
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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
22 citing papers in PubMed, 48 citations in OpenAlex.
- Stratification of systemic lupus erythematosus with IGHV4-34 in unswitched memory B cells.Rheumatology (Oxford, England) · 2025Article
- PI3Kγ in B cells promotes antibody responses and generation of antibody-secreting cells.Nature immunology · 2024Article
- Review
- Antigen presentation by B cells enables epitope spreading across an MHC barrier.Nature communications · 2023Article
- Endogenous complement-activating IgM is not required for primary antibody responses but promotes plasma cell differentiation and secondary antibody responses to a large particulate antigen in mice.Frontiers in immunology · 2023Article
- The role of the complement system in kidney glomerular capillary thrombosis.Frontiers in immunology · 2022Review
- Theiler's virus-induced demyelinating disease as an infectious model of progressive multiple sclerosis.Frontiers in molecular neuroscience · 2022Review
- Dynamic regulation of B cell complement signaling is integral to germinal center responses.Nature immunology · 2021Article
- Hijacking of the Host's Immune Surveillance Radars byFrontiers in immunology · 2021Review
- Linking signaling and selection in the germinal center.Immunological reviews · 2019Review
- Article
- Interaction of Serum-Derived and Internalized C3 With DNA in Human B Cells-A Potential Involvement in Regulation of Gene Transcription.Frontiers in immunology · 2019Article
- Novel identification and characterisation of Transient receptor potential melastatin 3 ion channels on Natural Killer cells and B lymphocytes: effects on cell signalling in Chronic fatigue syndrome/Myalgic encephalomyelitis patients.Biological research · 2016Article
- Article
- Requirement for complement in antibody responses is not explained by the classic pathway activator IgM.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Murine visceral leishmaniasis: IgM and polyclonal B-cell activation lead to disease exacerbation.European journal of immunology · 2010Article
- Uncoupling CD21 and CD19 of the B-cell coreceptor.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- B cell acquisition of antigen in vivo.Current opinion in immunology · 2009Review
- T cell-independent and toll-like receptor-dependent antigen-driven activation of autoreactive B cells.Immunity · 2008Article
- The classical complement pathway in transplantation: unanticipated protective effects of C1q and role in inductive antibody therapy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
B cells express complement receptors (CRs) that bind activated fragments of C3 and C4. Immunized CR knockout (KO) mice have lower antibody titers and smaller germinal centers (GCs), demonstrating the importance of CR signals for the humoral immune response. CR ligands were thought to be generated via complement fixation mediated by preexisting "natural" IgM or early Ab from inefficiently activated B cells. This concept was recently challenged by a transgenic (Tg) mouse model that lacks circulating antibody but still retains membrane IgM (mIgM) and mounts normal immune responses. To test whether CR ligands could be generated by the B cell receptor (BCR) itself, we generated similar mice carrying a mutated mIgM that was defective in C1q binding. We found that B cells from such mutant mice do not deposit C3 on B cells upon BCR ligation, in contrast to B cells from mIgM mice. This has implications for the immune response: the mutant mice have smaller GCs than mIgM mice, and they are particularly deficient in the maintenance of the GC response. These results demonstrate a new BCR-dependent pathway that is sufficient and perhaps necessary to provide a CR1/2 ligand that promotes efficient B cell activation.
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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.