ArticleProceedings of the National Academy of Sciences of the United States of America2011
Interleukin-2 inhibits FMS-like tyrosine kinase 3 receptor ligand (flt3L)-dependent development and function of conventional and plasmacytoid dendritic cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Epigenetics of Dendritic Cells in Tumor Immunology.Cancers · 2022Review
- Characterization of the cytokine storm reflects hyperinflammatory endothelial dysfunction in COVID-19.The Journal of allergy and clinical immunology · 2021Article
- Combination of radiotherapy and suppression of Tregs enhances abscopal antitumor effect and inhibits metastasis in rectal cancer.Journal for immunotherapy of cancer · 2020Article
- FGL2 promotes tumor progression in the CNS by suppressing CD103Nature communications · 2019Article
- Dynamical Analysis of the Regulatory Network Controlling Natural Killer Cells Differentiation.Frontiers in physiology · 2018Article
- Type 1 diabetes genetic susceptibility and dendritic cell function: potential targets for treatment.Journal of leukocyte biology · 2016Review
- Flow cytometric gating for spleen monocyte and DC subsets: differences in autoimmune NOD mice and with acute inflammation.Journal of immunological methods · 2016Article
- The Role of Dendritic Cell Subsets and Innate Immunity in the Pathogenesis of Type 1 Diabetes and Other Autoimmune Diseases.Frontiers in immunology · 2015Review
- Interleukin-2-mediated inhibition of dendritic cell development correlates with decreased CD135 expression and increased monocyte/macrophage precursors.Immunology · 2014Article
- Accumulation of FLT3(+) CD11c (+) dendritic cells in psoriatic lesions and the anti-psoriatic effect of a selective FLT3 inhibitor.Immunologic research · 2014Article
- Increased IFN-α-producing plasmacytoid dendritic cells (pDCs) in human Th1-mediated type 1 diabetes: pDCs augment Th1 responses through IFN-α production.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- CD8+ dendritic cell-mediated tolerance of autoreactive CD4+ T cells is deficient in NOD mice and can be corrected by blocking CD40L.Journal of leukocyte biology · 2014Article
- Immune heterogeneity in neuroinflammation: dendritic cells in the brain.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Review
- The equivalents of human blood and spleen dendritic cell subtypes can be generated in vitro from human CD34(+) stem cells in the presence of fms-like tyrosine kinase 3 ligand and thrombopoietin.Cellular & molecular immunology · 2012Article
- Spontaneous autoimmunity in the absence of IL-2 is driven by uncontrolled dendritic cells.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- The role of interleukin-2 during homeostasis and activation of the immune system.Nature reviews. Immunology · 2012Review
- Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Steady-state development of plasmacytoid dendritic cells (pDCs) and conventional dendritic cells (cDCs) requires the ligand for FMS-like tyrosine kinase 3 receptor (flt3L), but little is known about how other cytokines may also control this process. In this study, we show that IL-2 inhibits the development of both pDCs and cDCs from bone marrow cells under flt3L stimulation, by acting on lineage(-) flt3(+) precursors. This inhibition of DC development by IL-2 requires IL-2Rα and IL2Rβ. IL-2Rα is specifically expressed in one stage of the DC precursor: the monocyte and DC progenitors (MDPs). Furthermore, more MDPs are found in flt3L-stimulated bone marrow cultures when IL-2 is present, suggesting that IL-2 may be inhibiting DC development at the MDP stage. Consistent with our in vitro findings, we observe that nonobese diabetic (NOD) mice, which express less IL-2 compared with diabetes-resistant NOD.Idd3/5 mice, have more splenic pDCs. Additionally, DCs developed in vitro in the presence of flt3L and IL-2 display reduced ability to stimulate T-cell proliferation compared with DCs developed in the presence of flt3L alone. Although the addition of IL-2 does not increase the apoptosis of DCs during their development, DCs developed in the presence of IL-2 are more prone to apoptosis upon interaction with T cells. Together our data show that IL-2 can inhibit both the development and the function of DCs. This pathway may have implications for the loss of immune tolerance: Reduced IL-2 signaling may lead to increased DC number and T-cell stimulatory capacity.
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