ArticleThe Journal of clinical investigation2002
IL-15, a survival factor for kidney epithelial cells, counteracts apoptosis and inflammation during nephritis.
Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 90 citations in OpenAlex.
- Assessment of Interleukin-15 (IL-15) Concentration in Children with Cystic Kidney Disease.Biomedicines · 2026Article
- Natural killer cells in kidney immune surveillance, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- Stroma-specific IL-15 coordinates epithelial IL-15Rα to promote intestinal epithelial repair.Science China. Life sciences · 2026Article
- Circulating inflammatory proteins are elevated in type 1 and type 2 diabetes and associated to complications.Diabetes, obesity & metabolism · 2025Article
- BK Polyomavirus and acute kidney injury in transplant recipients: signaling pathways and molecular mechanisms.Virology journal · 2025Review
- Mechanisms Underlying the Impact of Interleukin Family on Acute Kidney Injury: Pathogenesis, Progression, and Therapy.Research (Washington, D.C.) · 2025Review
- Cognate antigen-independent differentiation of resident memory T cells in chronic kidney disease.American journal of physiology. Renal physiology · 2024Article
- Protective Role of the Podocyte IL-15 / STAT5 Pathway in Focal Segmental Glomerulosclerosis.Kidney international reports · 2024Article
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- IL-15 in T-Cell Responses and Immunopathogenesis.Immune network · 2024Review
- Assessment of Interleukin-15 (IL-15) Concentration in Children with Idiopathic Nephrotic Syndrome.International journal of molecular sciences · 2023Article
- Article
- Effector Memory-Expressing CD45RA (TEMRA) CD8Journal of the American Society of Nephrology : JASN · 2022Article
- Article
- Harnessing IL-15 signaling to potentiate NK cell-mediated cancer immunotherapy.Trends in immunology · 2022Review
- IL-15 Prevents Renal Fibrosis by Inhibiting Collagen Synthesis: A New Pathway in Chronic Kidney Disease?International journal of molecular sciences · 2021Article
- A therapeutic oxygen carrier isolated from Arenicola marina decreased P. gingivalis induced inflammation and tissue destruction.Scientific reports · 2020Article
- Administration of Interleukin-15 Peptide Improves Cardiac Function in a Mouse Model of Myocardial Infarction.Journal of cardiovascular pharmacology · 2020Article
- Inhibition of TGF-International journal of cell biology · 2019Article
- Therapeutic Effects of Tangshen Formula on Diabetic Nephropathy inJournal of diabetes research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
IL-15, a T cell growth factor, has been linked to exacerbating autoimmune diseases and allograft rejection. To test the hypothesis that IL-15-deficient (IL-15-/-) mice would be protected from T cell-dependent nephritis, we induced nephrotoxic serum nephritis (NSN) in IL-15-/- and wild-type (IL-15+/+) C57BL/6 mice. Contrary to our expectations, IL-15 protects the kidney during this T cell-dependent immunologic insult. Tubular, interstitial, and glomerular pathology and renal function are worse in IL-15-/- mice during NSN. We detected a substantial increase in tubular apoptosis in IL-15-/- kidneys. Moreover, macrophages and CD4 T cells are more abundant in the interstitia and glomeruli in IL-15-/- mice. This led us to identify several mechanisms responsible for heightened renal injury in the absence of IL-15. We now report that IL-15 and the IL-15 receptor (alpha, beta, gamma chains) are constitutively expressed in normal tubular epithelial cells (TECs). IL-15 is an autocrine survival factor for TECs. TEC apoptosis induced with anti-Fas or actinomycin D is substantially greater in IL-15-/- than in wild-type TECs. Moreover, IL-15 decreases the induction of a nephritogenic chemokine, MCP-1, that attracts leukocytes into the kidney during NSN. Taken together, we suggest that IL-15 is a therapeutic for tubulointerstitial and glomerular kidney diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.