ArticleJCI insight2020
Pathogenic, glycolytic PD-1+ B cells accumulate in the hypoxic RA joint.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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.
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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.
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Who cites it
36 citing papers in PubMed, 67 citations in OpenAlex.
- A guide to B cell metabolism.Nature reviews. Immunology · 2026Review
- Hypoxia as an amplifier of synovial inflammation in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity.Cellular & molecular immunology · 2026Review
- Review
- IgA-Producing B Cells Exert Regulatory Function through Granzyme B in Kidney Allograft Tolerance.Kidney360 · 2026Observational
- TIGITFrontiers in immunology · 2026Review
- Fatty Acid Metabolic Reprogramming in Rheumatoid Arthritis: Integrating Inflammation, Resolution Failure, and Joint Destruction.Journal of inflammation research · 2026Review
- Transitional and CD21BMC rheumatology · 2025Article
- [Bioinformatics analysis of oxidative stress and immune infiltration in rheumatoid arthritis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- B cell immunometabolism in health and disease.Nature immunology · 2025Review
- Citrullinated peptides as drug candidates for rheumatoid arthritis.Frontiers in immunology · 2025Review
- Lactate and lactylation: emerging roles in autoimmune diseases and metabolic reprogramming.Frontiers in immunology · 2025Review
- SHIP1 deficiency causes inflammation-dependent retardation in skeletal growth.Life science alliance · 2024Article
- Unraveling the complex interplay between anti-tumor immune response and autoimmunity mediated by B cells and autoantibodies in the era of anti-checkpoint monoclonal antibody therapies.Frontiers in immunology · 2024Review
- 2P-FLIM unveils time-dependent metabolic shifts during osteogenic differentiation with a key role of lactate to fuel osteogenesis via glutaminolysis identified.Stem cell research & therapy · 2023Article
- Mitochondria as disease-relevant organelles in rheumatoid arthritis.Clinical and experimental immunology · 2023Article
- A review of the pleiotropic actions of the IFN-inducible CXC chemokine receptor 3 ligands in the synovial microenvironment.Cellular and molecular life sciences : CMLS · 2023Review
- Immune checkpoints in rheumatoid arthritis: progress and promise.Frontiers in immunology · 2023Review
- Age/autoimmunity-associated B cells in inflammatory arthritis: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Computational approaches in rheumatic diseases - Deciphering complex spatio-temporal cell interactions.Computational and structural biotechnology journal · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While autoantibodies are used in the diagnosis of rheumatoid arthritis (RA), the function of B cells in the inflamed joint remains elusive. Extensive flow cytometric characterization and SPICE algorithm analyses of single-cell synovial tissue from patients with RA revealed the accumulation of switched and double-negative memory programmed death-1 receptor-expressing (PD-1-expressing) B cells at the site of inflammation. Accumulation of memory B cells was mediated by CXCR3, evident by the observed increase in CXCR3-expressing synovial B cells compared with the periphery, differential regulation by key synovial cytokines, and restricted B cell invasion demonstrated in response to CXCR3 blockade. Notably, under 3% O2 hypoxic conditions that mimic the joint microenvironment, RA B cells maintained marked expression of MMP-9, TNF, and IL-6, with PD-1+ B cells demonstrating higher expression of CXCR3, CD80, CD86, IL-1β, and GM-CSF than their PD-1- counterparts. Finally, following functional analysis and flow cell sorting of RA PD-1+ versus PD-1- B cells, we demonstrate, using RNA-Seq and emerging fluorescence lifetime imaging microscopy of cellular NAD, a significant shift in metabolism of RA PD-1+ B cells toward glycolysis, associated with an increased transcriptional signature of key cytokines and chemokines that are strongly implicated in RA pathogenesis. Our data support the targeting of pathogenic PD-1+ B cells in RA as a focused, novel therapeutic option.
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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.