ArticleJournal of the American Society of Nephrology : JASN2017
IL-33-Mediated Expansion of Type 2 Innate Lymphoid Cells Protects from Progressive Glomerulosclerosis.
Article in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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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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Who cites it
68 citing papers in PubMed, 109 citations in OpenAlex.
- Article
- Spatial and Phenotypic Heterogeneity of ILC Subsets in Mouse Lung Under Type 2 Inflammatory Conditions.European journal of immunology · 2026Article
- Cytokine-mediated, organ-specific immune modulation and dysregulation of innate lymphocytes in sepsis.Seminars in immunopathology · 2026Review
- Beyond the alarm: unveiling the multifaceted role of IL-33 in kidney disease.Frontiers in immunology · 2026Review
- ILC imbalance - a new piece in the gut-kidney axis puzzle.Frontiers in immunology · 2026Review
- Engineered Neuromedin U Promotes Type 2 Innate Immunity and Renoprotection in Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Innate Lymphoid Cells Are the Rheostat of Immune Response in the Kidney.Journal of cellular and molecular medicine · 2025Review
- Advances in Nano-Immunomodulatory Systems for the Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Lymphocytes and innate immune cells in acute kidney injury and repair.Nature reviews. Nephrology · 2024Review
- Dual Time-Dependent Effects of Interleukin-33 Administration on the Kidney Postmyocardial Infarction.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2024Article
- Renal IL-23-Dependent Type 3 Innate Lymphoid Cells Link Crystal-induced Intrarenal Inflammasome Activation with Kidney Fibrosis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Stress-induced eosinophil activation contributes to postoperative morbidity and mortality after lung resection.Science translational medicine · 2024Article
- The protective roles of integrin α4β7 and Amphiregulin-expressing innate lymphoid cells in lupus nephritis.Cellular & molecular immunology · 2024Article
- Impact of Organ Donor Pretreatment With Anti-Thymocyte Globulin in a Murine Model of Allogenic Kidney Transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2024Article
- Retinoic acid drives intestine-specific adaptation of effector ILC2s originating from distant sites.The Journal of experimental medicine · 2023Article
- Exploring the significance of interleukin-33/ST2 axis in minimal change disease.Scientific reports · 2023Article
- Protective and pathogenic functions of innate lymphoid cells in transplantation.Clinical and experimental immunology · 2023Review
- Nuclear IL-33 in Fibroblasts Promotes Skin Fibrosis.The Journal of investigative dermatology · 2023Article
- Group 2 innate lymphoid cells protect mouse heart from myocardial infarction injury via interleukin 5, eosinophils, and dendritic cells.Cardiovascular research · 2023Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate lymphoid cells (ILCs) have an important role in the immune system's response to different forms of infectious and noninfectious pathologies. In particular, IL-5- and IL-13-producing type 2 ILCs (ILC2s) have been implicated in repair mechanisms that restore tissue integrity after injury. However, the presence of renal ILCs in humans has not been reported. In this study, we show that ILC populations are present in the healthy human kidney. A detailed characterization of kidney-residing ILC populations revealed that IL-33 receptor-positive ILC2s are a major ILC subtype in the kidney of humans and mice. Short-term IL-33 treatment in mice led to sustained expansion of IL-33 receptor-positive kidney ILC2s and ameliorated adriamycin-induced glomerulosclerosis. Furthermore, the expansion of ILC2s modulated the inflammatory response in the diseased kidney in favor of an anti-inflammatory milieu with a reduction of pathogenic myeloid cell infiltration and a marked accumulation of eosinophils that was required for tissue protection. In summary, kidney-residing ILC2s can be effectively expanded in the mouse kidney by IL-33 treatment and are central regulators of renal repair mechanisms. The presence of ILC2s in the human kidney tissue identifies these cells as attractive therapeutic targets for CKD in humans.
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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.