ArticleJournal of innate immunity2022
T-Cell Immune Imbalance in Rheumatoid Arthritis Is Associated with Alterations in NK Cells and NK-Like T Cells Expressing CD38.
Article in Journal of innate immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The trial behind it
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- CD38+ NK cells: novel players in immunoregulation.Frontiers in immunology · 2026Review
- Liver-joint axis: Hepatitis B virus as a contributor to rheumatoid arthritis pathogenesis.Virulence · 2025Review
- Metabolic regulation of Th17 and Treg cell balance by the mTOR signaling.Metabolism open · 2025Review
- Increased Sirtuin 6 Activity in Tumor Cells Can Prompt CD4-Positive T-Cell Differentiation Into Regulatory T Cells and Impede Immune Surveillance in the Microenvironment.World journal of oncology · 2025Article
- Moxibustion Regulates the Expression of T Cells in Rheumatoid Arthritis Through Tim-3/Gal-9 Signaling Pathway.Rejuvenation research · 2025Article
- CD38 modulates cytokine secretion by NK cells through the Sirt1/NF-κB pathway, suppressing immune surveillance in colorectal cancer.Scientific reports · 2024Article
- Review
- Article
- Immune Cell-Derived Exosomes in Inflammatory Disease and Inflammatory Tumor Microenvironment: A Review.Journal of inflammation research · 2024Review
- Overexpression of circulating CD38+ NK cells in colorectal cancer was associated with lymph node metastasis and poor prognosis.Frontiers in oncology · 2024Article
- Overview of mechanisms and novel therapies on rheumatoid arthritis from a cellular perspective.Frontiers in immunology · 2024Review
- Article
- Article
- Targeting CD38 in Neoplasms and Non-Cancer Diseases.Cancers · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCD38+ NK (CD3- CD16+ CD38+ CD56+) cells were increased in rheumatoid arthritis (RA), which suppressed Treg cell differentiation. This study explored how CD38+ NK cells regulated CD4+ T-cell differentiation into Treg cells in RA.
methodsProportions of CD38+ NK cells and their counterpart CD38+ NK-like T (CD3+ CD16+ CD38+ CD56+) cells were measured in RA and rats with collagen-induced arthritis (CIA). CD38+ NK cells and CD38+ NK-like T cells were cocultured with CD4+ T cells, respectively.
resultsA significantly increased proportion of CD38+ NK cells and a decreased proportion of CD38+ NK-like T cells were detected in RA and CIA blood and synovial fluids. When CD4+ T cells were cocultured with CD38+ NK cells, mammalian target of rapamycin (mTOR) signaling was activated, and Th1/Th2 and Th17/Treg ratios were increased. When CD38+ NK cells were pretreated with anti-CD38 antibody, Treg cell proportion was increased, and Th1/Th2 and Th17/Treg ratios were decreased. CD38+ NK-like T cells showed the opposite results. CD38+ NK cells and CD38+ NK-like-T cells activated differential gene expressions and pathways in CD4+ T cells and initiated Th1 and Th2 cell differentiation by differential gene nodes.
conclusionsThis study suggest that the high CD38+ NK cell proportion and low CD38+ NK-like T cell proportion in RA suppress Treg cell differentiation by stimulating mTOR signaling in CD4+ T cells, which consequentially disturbs the immune tolerance.
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Registered trials
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