ReviewClinical reviews in allergy & immunology2014
Unmet needs in autoimmunity and potential new tools.
Review in Clinical reviews in allergy & immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 12 citations in OpenAlex.
- The causal relationship between sarcoidosis and autoimmune diseases: a bidirectional Mendelian randomization study in FinnGen.Frontiers in immunology · 2024Article
- The roles of PPARγ and its agonists in autoimmune diseases: A comprehensive review.Journal of autoimmunity · 2020Review
- Epigenetics and Primary Biliary Cirrhosis: a Comprehensive Review and Implications for Autoimmunity.Clinical reviews in allergy & immunology · 2016Review
- The Inflammatory Response in Psoriasis: a Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- Critical Link Between Epigenetics and Transcription Factors in the Induction of Autoimmunity: a Comprehensive Review.Clinical reviews in allergy & immunology · 2016Review
- CD24: from a Hematopoietic Differentiation Antigen to a Genetic Risk Factor for Multiple Autoimmune Diseases.Clinical reviews in allergy & immunology · 2016Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The term "autoimmunity" refers to a pathological condition in which the immunological tolerance of self-antigens is broken through, cross-reactive T cells are activated, and autoantibodies are produced by B cells. The intricate interplay among those aberrantly activated immune cells as well as inflammatory cytokines secreted by them contributes to the development of proinflammatory cascade which eventually leads to the occurrence of autoimmune diseases (AIDs) and organ damage. Autoimmune diseases occupy a broad spectrum of human diseases with more than 70 different disorders and afflict approximately 5-8 % of the world's population. AIDs can be categorized into organ-specific and systemic. Although the exact mechanism of AIDs remains elusive, it is generally believed that both genetic polymorphism and environmental exposure are involved in the development of AIDs. Aberrant epigenetic marks are also identified in patients with AIDs. In addition, dysregulation of innate immune system and molecular mimicry are indicated to play important roles in the initiation and maintenance of autoreactive inflammation. Based on the progress made in elucidating molecular mechanisms underlying AIDs, novel biomarkers for prediction, early diagnosis, prognosis and treatment response, and therapeutic strategies are proposed, which represents a promising future in the battle against AIDs. However, challenges remain regarding the clinical application of these potential new tools.
Indexed as
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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.