ReviewNature reviews. Rheumatology2015
New players driving inflammation in monogenic autoinflammatory diseases.
Review in Nature reviews. Rheumatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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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
35 citing papers in PubMed, 64 citations in OpenAlex.
- Review
- NETosis: an emerging therapeutic target in renal diseases.Frontiers in immunology · 2023Review
- Case report:Frontiers in pediatrics · 2023Article
- Loss of Function Mutation in ELF4 Causes Autoinflammatory and Immunodeficiency Disease in Human.Journal of clinical immunology · 2022Article
- Deficiency of Human Adenosine Deaminase Type 2 - A Diagnostic Conundrum for the Hematologist.Frontiers in immunology · 2022Review
- Allogeneic Hematopoietic Cell Transplantation for Patients With Deficiency of Adenosine Deaminase 2 (DADA2): Approaches, Obstacles and Special Considerations.Frontiers in immunology · 2022Review
- Proteomic Signatures of Monocytes in Hereditary Recurrent Fevers.Frontiers in immunology · 2022Article
- Autoinflammation and autoimmunity across rheumatic and musculoskeletal diseases.Nature reviews. Rheumatology · 2021Review
- Hematopoietic Cell Transplantation Cures Adenosine Deaminase 2 Deficiency: Report on 30 Patients.Journal of clinical immunology · 2021Article
- Vasculitis, Autoimmunity, and Cytokines: How the Immune System Can Harm the Brain.International journal of environmental research and public health · 2021Review
- The Spectrum of the Deficiency of Adenosine Deaminase 2: An Observational Analysis of a 60 Patient Cohort.Frontiers in immunology · 2021Observational
- A Novel Mutation in the NBD Domain ofFrontiers in immunology · 2021Article
- Epigenetic Mechanisms of Inflammasome Regulation.International journal of molecular sciences · 2020Review
- Inflammasomes and Proteostasis Novel Molecular Mechanisms Associated With Atrial Fibrillation.Circulation research · 2020Review
- Catestatin improves insulin sensitivity by attenuating endoplasmic reticulum stress:Computational and structural biotechnology journal · 2020Article
- Low Evolutionary Selection Pressure in Senescence Does Not Explain the Persistence of Aβ in the Vertebrate Genome.Frontiers in aging neuroscience · 2019Review
- [Focus on pediatric rheumatic and immune diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Article
- Chemical stresses fail to mimic the unfolded protein response resulting from luminal load with unfolded polypeptides.The Journal of biological chemistry · 2018Article
- Aberrant tRNA processing causes an autoinflammatory syndrome responsive to TNF inhibitors.Annals of the rheumatic diseases · 2018Article
- Neither hereditary periodic fever nor periodic fever, aphthae, pharingitis, adenitis: Undifferentiated periodic fever in a tertiary pediatric center.World journal of clinical pediatrics · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic autoinflammatory diseases are caused by abnormal activation of the cells that mediate innate immunity. In the past two decades, single-gene defects in different pathways, driving clinically distinct autoinflammatory syndromes, have been identified. Studies of these aberrant pathways have substantially advanced understanding of the cellular mechanisms that contribute to mounting effective and balanced innate immune responses. For example, mutations affecting the function of cytosolic immune sensors known as inflammasomes and the IL-1 signalling pathway can trigger excessive inflammation. A surge in discovery of new genes associated with autoinflammation has pointed to other mechanisms of disease linking innate immune responses to a number of basic cellular pathways, such as maintenance of protein homeostasis (proteostasis), protein misfolding and clearance, endoplasmic reticulum stress and mitochondrial stress, metabolic stress, autophagy and abnormalities in differentiation and development of myeloid cells. Although the spectrum of autoinflammatory diseases has been steadily expanding, a substantial number of patients remain undiagnosed. Next-generation sequencing technologies will be instrumental in finding disease-causing mutations in as yet uncharacterized diseases. As more patients are reported to have clinical features of autoinflammation and immunodeficiency or autoimmunity, the complex interactions between the innate and adaptive immune systems are unveiled.
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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.