ArticlePloS one2012
The myeloid receptor PILRβ mediates the balance of inflammatory responses through regulation of IL-27 production.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 23 citations in OpenAlex.
- Biomarker identification for Alzheimer's disease through integration of comprehensive Mendelian randomization and proteomics data.Journal of translational medicine · 2025Article
- Spatial transcriptomics identifies RBM39 as a gene aiScience · 2024Article
- Single-cell transcriptomic analysis of radiation-induced lung injury in rat.Biomolecules & biomedicine · 2024Article
- PILRB potentiates the PI3K/AKT signaling pathway and reprograms cholesterol metabolism to drive gastric tumorigenesis and metastasis.Cell death & disease · 2024Article
- PILRA polymorphism modifies the effect of APOE4 and GM17 on Alzheimer's disease risk.Scientific reports · 2022Article
- Microglia in Alzheimer's Disease: An Unprecedented Opportunity as Prospective Drug Target.Molecular neurobiology · 2022Review
- Microglia in Alzheimer's Disease: a Key Player in the Transition Between Homeostasis and Pathogenesis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
- Innate Immunity in Age-Related Macular Degeneration.Advances in experimental medicine and biology · 2021Article
- Integrated Analysis Revealed Prognostic Factors for Prostate Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Blood flow guides sequential support of neutrophil arrest and diapedesis by PILR-β1 and PILR-α.eLife · 2019Article
- Paired Ig-Like Type 2 Receptor-Derived Agonist Ligands Ameliorate Inflammatory Reactions by Downregulating β1 Integrin Activity.Molecules and cells · 2016Article
- Maternal age effects on myometrial expression of contractile proteins, uterine gene expression, and contractile activity during labor in the rat.Physiological reports · 2015Article
- PILRα and PILRβ have a siglec fold and provide the basis of binding to sialic acid.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Paired immunoglobulin-like receptors beta, PILRβ, and alpha, PILRα, are related to the Siglec family of receptors and are expressed primarily on cells of the myeloid lineage. PILRβ is a DAP12 binding partner expressed on both human and mouse myeloid cells. The potential ligand, CD99, is found on many cell types, such as epithelial cells where it plays a role in migration of immune cells to sites of inflammation. Pilrb deficient mice were challenged with the parasite Toxoplasma gondii in two different models of infection induced inflammation; one involving the establishment of chronic encephalitis and a second mimicking inflammatory bowel disease in order to understand the potential role of this receptor in persistent inflammatory responses. It was found that in the absence of activating signals from PILRβ, antigen-presenting cells (APCs) produced increased amounts of IL-27, p28 and promoted IL-10 production in effector T cells. The sustained production of IL-27 led ultimately to enhanced survival after challenge due to dampened immune pathology in the gut. Similar protection was also observed in the CNS during chronic T. gondii infection after i.p. challenge again providing evidence that PILRβ is important for regulating aberrant inflammatory responses.
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.