ArticleThe Journal of experimental medicine2009
Role of breast regression protein 39 (BRP-39)/chitinase 3-like-1 in Th2 and IL-13-induced tissue responses and apoptosis.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers, 4 of them syntheses that pooled it.
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.
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
242 citing papers in PubMed, 4 syntheses or guidelines pooled it, 442 citations in OpenAlex.
- Chitinase‑3 like‑protein‑1: A potential predictor of cardiovascular disease (Review).Molecular medicine reports · 2024Pooled it
- Association between YKL-40 and asthma: a systematic meta-analysis.Sleep & breathing = Schlaf & Atmung · 2022Pooled it
- Functional study of the association ofBioscience reports · 2019Pooled it
- The relation of circulating YKL-40 to levels and decline of lung function in adult life.Respiratory medicine · 2013Pooled it
- Plasma YKL-40 is associated with prognosis in patients with metastatic pancreatic cancer receiving immune checkpoint inhibitors in combination with radiotherapy.Frontiers in immunology · 2023Trial
- Safety and effectiveness of neoadjuvant PD-1 inhibitor (toripalimab) plus chemotherapy in stage II-III NSCLC (LungMate 002): an open-label, single-arm, phase 2 trial.BMC medicine · 2022Trial
- Chitinase 3-like-1 and its receptors in Hermansky-Pudlak syndrome-associated lung disease.The Journal of clinical investigation · 2015Trial
- Plasma YKL-40 and all-cause mortality in patients with chronic obstructive pulmonary disease.BMC pulmonary medicine · 2013Trial
- Bispecific targeting of CHI3L1 and PD-1 as a therapeutic strategy for pulmonary fibrosis.JCI insight · 2026Article
- Article
- Serum Zonulin and Chitinase (CHI3L1) as Biomarkers of Intestinal Permeability and Disease Activity in Pediatric Celiac Disease.Children (Basel, Switzerland) · 2026Article
- Distinct immune landscapes characterize highly versus minimally invasive brain metastases.JCI insight · 2026Article
- Role of Chitinase 3-like-1 in Myelofibrosis via Fibroblast-Produced Extracellular Matrix Enhancement.Journal of cellular physiology · 2026Article
- Host Proteome Remodeling During Group A Streptococcus Skin Infection.Molecular & cellular proteomics : MCP · 2026Article
- CHI3L1 Is Associated With TP53 Signaling and Promotes Papillary Thyroid Carcinoma Progression.Cancer reports (Hoboken, N.J.) · 2026Article
- The CHI3L1-neutrophil axis drives immune suppression and breast cancer metastatic dissemination.JCI insight · 2026Article
- Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation.ImmunoTargets and therapy · 2026Article
- CHI3L1 promotes cell division through activation of RhoA in lung cancer cells.Cell communication and signaling : CCS · 2025Article
- Up-regulated chitinase-like protein-1 promotes tumour growth while physiological levels are protective.Life science alliance · 2025Article
- Generation of a Ym1 deficient mouse utilising CRISPR-Cas9 in CB6 embryos.Transgenic research · 2025Article
182 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Mouse breast regression protein 39 (BRP-39; Chi3l1) and its human homologue YKL-40 are chitinase-like proteins that lack chitinase activity. Although YKL-40 is expressed in exaggerated quantities and correlates with disease activity in asthma and many other disorders, the biological properties of BRP-39/YKL-40 have only been rudimentarily defined. We describe the generation and characterization of BRP-39(-/-) mice, YKL-40 transgenic mice, and mice that lack BRP-39 and produce YKL-40 only in their pulmonary epithelium. Studies of these mice demonstrated that BRP-39(-/-) animals have markedly diminished antigen-induced Th2 responses and that epithelial YKL-40 rescues the Th2 responses in these animals. The ability of interleukin13 to induce tissue inflammation and fibrosis was also markedly diminished in the absence of BRP-39. Mechanistic investigations demonstrated that BRP-39 and YKL-40 play an essential role in antigen sensitization and immunoglobulin E induction, stimulate dendritic cell accumulation and activation, and induce alternative macrophage activation. These proteins also inhibit inflammatory cell apoptosis/cell death while inhibiting Fas expression, activating protein kinase B/AKT, and inducing Faim 3. These studies establish novel regulatory roles for BRP-39/YKL-40 in the initiation and effector phases of Th2 inflammation and remodeling and suggest that these proteins are therapeutic targets in Th2- and macrophage-mediated disorders.
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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.