Evidence map›Paper›PMID 15067315›Full record

ArticleThe Journal of clinical investigation2004

Dysregulated LIGHT expression on T cells mediates intestinal inflammation and contributes to IgA nephropathy.

Jing Wang, Robert A Anders, Qiang Wu, Dacheng Peng, Judy H Cho, Yonglian Sun, Reda Karaliukas, Hyung-Sik Kang, Jerrold R Turner, Yang-Xin Fu

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 122 citations in OpenAlex.

  1. APRIL: spring forward also for IgA vasculitis nephritis in children.Pediatric nephrology (Berlin, Germany) · 2026
    Article
  2. Review
  3. Multiple circulating inflammatory proteins are associated with pathological lesions and kidney function decline in IgA nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Lessons from IgA Nephropathy Models.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Review
  12. Article
  13. IgA nephropathy associated with Crohn's disease.World journal of methodology · 2023
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Are there animal models of IgA nephropathy?Seminars in immunopathology · 2021
    Review
  20. Article

3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Jing WangDepartment of Pathology, University of Chicago, Chicago, Illinois 60637, USA.
Robert A Anders
Qiang Wu
Dacheng Peng
Judy H Cho
Yonglian Sun
Reda Karaliukas
Hyung-Sik Kang
Jerrold R Turner
Yang-Xin Fu
University of Chicago · USUniversity of Iowa · US

Funding

CARDIOVASCULAR PATHOPHYSIOLOGY &BIOCHEMISTRY TRAININGT32HL007237 · NHLBI · UNIVERSITY OF CHICAGO · PI GETZ, GODFREY SHALOM · 1985 to 2011
$5.0M
THE ROLE OF LYMPHOID MICROENVIRONMENT IN AUTOIMMUNITYR01DK058897 · NIDDK · UNIVERSITY OF CHICAGO · PI FU, YANG-XIN · 2001 to 2009
$2.9M
DEVELOPMENT AND FUNCTION OF LYMPHOID TISSUESR01HD037104 · NICHD · UNIVERSITY OF CHICAGO · PI FU, YANG-XIN · 1999 to 2003
$491k
NHLBI NIH HHS 5T32 HL07237NHLBI NIH HHS T32 HL007237NICHD NIH HHS HD-37104NICHD NIH HHS R01 HD037104NIDDK NIH HHS DK-58897NIDDK NIH HHS R01 DK058897
6 · The paper itself

Abstract

Whether and how T cells contribute to the pathogenesis of immunoglobulin A nephropathy (IgAN) has not been well defined. Here, we explore a murine model that spontaneously develops T cell-mediated intestinal inflammation accompanied by pathological features similar to those of human IgAN. Intestinal inflammation mediated by LIGHT, a ligand for lymphotoxin beta receptor (LTbetaR), not only stimulates IgA overproduction in the gut but also results in defective IgA transportation into the gut lumen, causing a dramatic increase in serum polymeric IgA. Engagement of LTbetaR by LIGHT is essential for both intestinal inflammation and hyperserum IgA syndrome in our LIGHT transgenic model. Impressively, the majority of patients with inflammatory bowel disease showed increased IgA-producing cells in the gut, elevated serum IgA levels, and severe hematuria, a hallmark of IgAN. These observations indicate the critical contributions of dysregulated LIGHT expression and intestinal inflammation to the pathogenesis of IgAN.

Indexed as

AnimalsComplement C3GastroenteritisGene Expression RegulationGlomerulonephritis, IGAImmunity, MucosalImmunoglobulin AInflammatory Bowel DiseasesKidney GlomerulusLymphotoxin beta ReceptorMembrane ProteinsMiceMice, TransgenicReceptors, Tumor Necrosis FactorT-LymphocytesTumor Necrosis Factor-alphaComplement C3Immunoglobulin ALTBR protein, humanLtbr protein, mouseLymphotoxin beta ReceptorMembrane ProteinsReceptors, Tumor Necrosis FactorTNFSF14 protein, humanTnfsf14 protein, mouseTumor Necrosis Factor-alphaTumor Necrosis Factor Ligand Superfamily Member 14

Identifiers

PMID15067315
PMCPMC362120
OpenAlexW2165054263

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.