ReviewCurrent opinion in immunology2018
Emerging areas for therapeutic discovery in SLE.
Review in Current opinion in immunology, 2018. 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.
- Colorimetry-Based Phosphate Measurement for Polymerase Elongation.BioMed research international · 2023Article
- The role of neutrophils in rheumatic disease-associated vascular inflammation.Nature reviews. Rheumatology · 2022Review
- Comparisons of Anti-dsDNA Antibody Detection Methods by Chemiluminescent Immunoassay and Enzyme-Linked Immunosorbent Assay in Systemic Lupus Erythematosus.Diagnostics (Basel, Switzerland) · 2021Article
- Clinical disease activity and flare in SLE: Current concepts and novel biomarkers.Journal of autoimmunity · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Recent advances in the field of autoimmunity have identified numerous dysfunctional pathways in Systemic Lupus Erythematosus (SLE), including aberrant clearance of nucleic-acid-containing debris and immune complexes, excessive innate immune activation leading to overactive type I IFN signalling, and abnormal B and T cell activation. On the background of genetic polymorphisms that reset thresholds for immune responses, multiple immune cells contribute to inflammatory amplification circuits. Neutrophils activated by immune complexes are a rich source of immunogenic nucleic acids. Identification of new B subsets suggests several mechanisms for induction of autoantibody producing effector cells. Disordered T cell regulation involves both CD4 and CD8 cells. An imbalance in immunometabolism in immune cells amplifies autoimmunity and inflammation. These new advances in understanding of disease pathogenesis provide fertile ground for therapeutic development.
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.