ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Fc gamma RIII and Fc gamma RIV are indispensable for acute glomerular inflammation induced by switch variant monoclonal antibodies.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 43 citations in OpenAlex.
- Patrolling monocytes mediate virus neutralizing IgG effector functions: beyond neutralization capacity.Frontiers in immunology · 2025Article
- Fcγ Receptor Heterogeneity in Leukocyte Functional Responses.Frontiers in immunology · 2017Review
- Experimentally-induced anti-myeloperoxidase vasculitis does not require properdin, MASP-2 or bone marrow-derived C5.The Journal of pathology · 2016Article
- Apoptotic Debris Accumulates on Hematopoietic Cells and Promotes Disease in Murine and Human Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Article
- Fcγ receptor III and Fcγ receptor IV on macrophages drive autoimmune valvular carditis in mice.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Dual role for Fcγ receptors in host defense and disease in Borrelia burgdorferi-infected mice.Frontiers in cellular and infection microbiology · 2014Article
- Fc-dependent depletion of tumor-infiltrating regulatory T cells co-defines the efficacy of anti-CTLA-4 therapy against melanoma.The Journal of experimental medicine · 2013Article
- Proteolysis breaks tolerance toward intact α345(IV) collagen, eliciting novel anti-glomerular basement membrane autoantibodies specific for α345NC1 hexamers.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Murine membranous nephropathy: immunization with α3(IV) collagen fragment induces subepithelial immune complexes and FcγR-independent nephrotic syndrome.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- The generation and evaluation of two panels of epitope-matched mouse IgG1, IgG2a, IgG2b and IgG3 antibodies specific for Plasmodium falciparum and Plasmodium yoelii merozoite surface protein 1-19 (MSP1(19)).Experimental parasitology · 2012Article
- The contribution of allergen-specific IgG to the development of th2-mediated airway inflammation.Journal of allergy · 2012Article
- L2pB1: a new player in autoimmunity.Molecular immunology · 2011Review
- FcγRIV deletion reveals its central role for IgG2a and IgG2b activity in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Alport alloantibodies but not Goodpasture autoantibodies induce murine glomerulonephritis: protection by quinary crosslinks locking cryptic α3(IV) collagen autoepitopes in vivo.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- CD96 targeted antibodies need not block CD96-CD155 interactions to promote NK cell anti-metastatic activity.OncoimmunologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 7 institutions in 4 countries.
Funding
Abstract
The relative ability of IgG subclasses to cause acute inflammation and the roles of specific effector mechanisms in this process are not clear. We explored this in an in vivo model of glomerular inflammation in the mouse. Trinitrophenol was planted on the glomerular basement membrane after conjugation to nephrotoxic Ab. The relative nephritogenicity of anti-trinitrophenol switch variant mAbs was then explored and shown to be IgG2a > IgG2b, with no disease caused by IgG1. Using knockout mice, we showed that FcgammaRIII was necessary for both neutrophil influx and glomerular damage induced by IgG2a and IgG2b. Surprisingly, IgG1 did not cause disease although it binds to FcgammaRIII. Using blocking Abs, we showed that this was explained by an additional requirement for FcgammaRIV, which does not bind to IgG1. IgG2a- or IgG2b-induced neutrophil influx was not affected by deficiency of either FcgammaRI or C3. Bone marrow chimeras were constructed to test the effect of combined deficiency of FcgammaRI and C3, and there was no effect on IgG2a- or IgG2b-mediated neutrophil influx. However, IgG2b-induced albuminuria and thrombosis were reduced in C3-deficient mice, showing an additional role for complement in IgG2b-mediated glomerular damage. The results show that IgG2a and IgG2b are the pathogenic subclasses in acute neutrophil-mediated glomerular inflammation, with an indispensable role for both FcgammaRIII and FcgammaRIV. Additionally, complement contributes to IgG2b-induced glomerular injury.
Indexed as
Identifiers
What OpenQuestion holds
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.