ArticleClinical reviews in allergy & immunology2019
Autoimmunity in 2018.
Article in Clinical reviews in allergy & immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- The Interplay of Autoimmune Disease, Cancer, and Immunity: Current Understanding and Therapeutic Prospects.International journal of hematology-oncology and stem cell research · 2025Review
- Activation Markers on B and T Cells and Immune Checkpoints in Autoimmune Rheumatic Diseases.International journal of molecular sciences · 2022Review
- STAT3 and SPI1, may lead to the immune system dysregulation and heterotopic ossification in ankylosing spondylitis.BMC immunology · 2022Article
- NF-κB signaling in inflammation and cancer.MedComm · 2021Review
- Epigenetic studies and pediatric research.Pediatric research · 2020Review
- Review
- Immunobiology of Atherosclerosis: A Complex Net of Interactions.International journal of molecular sciences · 2019Review
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
In the vast database of peer-reviewed articles, the number of 2018 papers published retrieved using the "autoimmunity" keyword remained unchanged compared with the brilliant results of 2017 while returning above a 5% share within the immunology field, after the brisk decrease of this ratio in 2017. As in the past 12 years, we have now searched PubMed for publications related to autoimmunity in the major immunology and autoimmunity peer-reviewed journals and provide here an arbitrary discussion of the major themes encountered. Once again, we are happy to notice that similarities between autoimmune diseases and the common mechanisms significantly outnumber differences. Some examples include data on Th17 cells, cytokines, or other mediators variably involved in the autoimmunity mechanisms such as BLIMP-1, IL-10, IFN, or NF-kB. The study of the microbiome remains central to autoimmunity development and data are being gathered in a growing number of conditions, similar to epigenetics and long non-coding RNA. In the cases of specific diseases, such as systemic lupus erythematosus, rheumatoid arthritis, or psoriatic arthritis, multiple encouraging findings underline the importance of a strict relationship between basic and clinical science to define new pathogenetic and therapeutic developments. Cumulatively, the present scenario of autoimmunity appears bright and should be regarded as one of the fastest growing in the scientific field of immunology, despite the enormous attention paid to cancer immune mechanisms. The parallel observation that the rheumatology therapeutic pipeline is second only to oncology increases the hopes that more and more patients will be satisfactorily treated in the near future.
Indexed as
Identifiers
31168760What 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.