ReviewImmunologic research2003
Mechanisms of autoimmunity.
Review in Immunologic research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- T cells, murine chronic graft-versus-host disease and autoimmunity.Journal of autoimmunity · 2012Review
- Increased expression of human T-cell immunoglobulin- and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus.Cellular & molecular immunology · 2010Article
- Is there a role for rituximab in the treatment of idiopathic childhood nephrotic syndrome?Pediatric nephrology (Berlin, Germany) · 2007Article
- Understanding the pathogenesis of psoriasis, psoriatic arthritis, and autoimmunity via a fusion of molecular genetics and immunology.Immunologic research · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmunity results from the failure of self-tolerance of the adaptive immune system. The reactivity of antibodies and T cells against endogenous antigens frequently causes organ damage, and consequent autoimmune disease. Systemic lupus erythematosus (SLE) is an extreme example of such a breakdown of tolerance. Our studies with spontaneous genetic mouse models of SLE and an experimentally induced model have elucidated many of the underlying cellular and genetic mechanisms of this immune dysregulation. We find that the B cell plays a key central role in this process and represents an attractive target for therapeutic intervention.
Indexed as
Identifiers
12857969What 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.