ReviewJournal of biomedicine & biotechnology2011
Role of PIR-B in autoimmune glomerulonephritis.
Review in Journal of biomedicine & biotechnology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 30 citations in OpenAlex.
- Claudins interact with LILRB immune inhibitory receptors to promote myeloid immunosuppression in cancer.Science immunology · 2026Article
- Oligomeric cystatin C supports the immunosuppressive activity of myeloid cells through interaction with inhibitory receptors.Signal transduction and targeted therapy · 2025Article
- Eph Receptors Activate Myeloid Checkpoint Receptor LILRB5 to Support Tumor Development.Cancer immunology research · 2025Article
- The dualistic role of Lyn tyrosine kinase in immune cell signaling: implications for systemic lupus erythematosus.Frontiers in immunology · 2024Review
- LILRB3 supports acute myeloid leukemia development and regulates T-cell antitumor immune responses through the TRAF2-cFLIP-NF-κB signaling axis.Nature cancer · 2021Article
- Leukocyte immunoglobulin-like receptor subfamily B: therapeutic targets in cancer.Antibody therapeutics · 2021Review
- Human Leucocyte Antigen G and Murine Qa-2 Are Critical for Myeloid Derived Suppressor Cell Expansion and Activation and for Successful Pregnancy Outcome.Frontiers in immunology · 2021Article
- CD72 is a Negative Regulator of B Cell Responses to Nuclear Lupus Self-antigens and Development of Systemic Lupus Erythematosus.Immune network · 2019Review
- CAMKs support development of acute myeloid leukemia.Journal of hematology & oncology · 2018Article
- Ligand Recognition Determines the Role of Inhibitory B Cell Co-receptors in the Regulation of B Cell Homeostasis and Autoimmunity.Frontiers in immunology · 2018Review
- New Insights Into the Role of Qa-2 and HLA-G Non-classical MHC-I Complexes in Malignancy.Frontiers in immunology · 2018Review
- Review
- B-cell tolerance and autoimmunity.F1000Research · 2017Review
- CD72 negatively regulates B lymphocyte responses to the lupus-related endogenous toll-like receptor 7 ligand Sm/RNP.The Journal of experimental medicine · 2016Article
- Leukocyte Ig-Like Receptors - A Model for MHC Class I Disease Associations.Frontiers in immunology · 2016Review
- Inhibitory leukocyte immunoglobulin-like receptors: Immune checkpoint proteins and tumor sustaining factors.Cell cycle (Georgetown, Tex.) · 2016Review
- Distribution of paired immunoglobulin-like receptor B in the nervous system related to regeneration difficulties after unilateral lumbar spinal cord injury.Neural regeneration research · 2015Article
- The ITIM-containing receptor LAIR1 is essential for acute myeloid leukaemia development.Nature cell biology · 2015Article
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- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PIR-B, an inhibitory receptor expressed on murine B cells and myeloid cells, regulates humoral and cellular immune responses via its constitutive binding to the ligand, MHC class I molecules, on the same cells (cis) or on different cells (trans). Although it has been speculated that PIR-B is important for maintaining peripheral tolerance, PIR-B single deficiency does not cause overt autoimmune diseases. Recently, however, the combination of its deficiency with the Fas lpr mutation was found to result in augmented production of autoantibodies such as IgG rheumatoid factor and anti-DNA IgG, leading to glomerulonephritis in mice. Although the precise molecular mechanism for the overall scenario is unclear, PIR-B was found to suppress TLR9-mediated production of naturally autoreactive antibodies by innate B cells or B-1 cells by inhibiting the activation of Bruton's tyrosine kinase. Thus, PIR-B is an important regulator of innate immunity mediated by TLR9 in B-1 cells, which can otherwise provoke autoimmunity when overactivated.
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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.