Evidence map›Paper›PMID 29985168›Full record

ArticleThe Journal of clinical investigation2018

Bowman's capsule provides a protective niche for podocytes from cytotoxic CD8+ T cells.

Anqun Chen, Kyung Lee, Vivette D D'Agati, Chengguo Wei, Jia Fu, Tian-Jun Guan, John Cijiang He, Detlef Schlondorff, Judith Agudo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 83 citations in OpenAlex.

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  8. Article
  9. The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Anqun ChenDivision of Nephrology, Zhongshan Hospital, affiliated with Xiamen University, Xiamen, Fujian Province, China.
Kyung LeeDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Vivette D D'AgatiDepartment of Pathology, Columbia University Medical Center, New York, New York, USA.
Chengguo WeiDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Jia FuDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Tian-Jun GuanDivision of Nephrology, Zhongshan Hospital, affiliated with Xiamen University, Xiamen, Fujian Province, China.
John Cijiang HeDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Detlef SchlondorffDepartment of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Judith AgudoInstitute of Precision Immunology, Icahn School of Medicine at Mount Sinai, New York New York, USA.
Icahn School of Medicine at Mount Sinai · USZhongshan Hospital of Xiamen University · CNColumbia University Irving Medical Center · USJames J. Peters VA Medical Center · US

Funding

Cellular and molecular mechanisms of retinoids in podocytesR01DK078897 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2007 to 2018
$3.6M
The Role of LRG1 in Diabetic Kidney DiseaseR01DK117913 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Bhaskar Chandra Das, Kyung Lee · 2018 to 2026
$2.6M
NIDDK NIH HHS R01 DK078897NIDDK NIH HHS R01 DK117913
6 · The paper itself

Abstract

T cells play a key role in immune-mediated glomerulonephritis, but how cytotoxic T cells interact with podocytes remains unclear. To address this, we injected EGFP-specific CD8+ T cells from just EGFP death inducing (Jedi) mice into transgenic mice with podocyte-specific expression of EGFP. In healthy mice, Jedi T cells could not access EGFP+ podocytes. Conversely, when we induced nephrotoxic serum nephritis (NTSN) and injected Jedi T cells, EGFP+ podocyte transgenic mice showed enhanced proteinuria and higher blood urea levels. Morphometric analysis showed greater loss of EGFP+ podocytes, which was associated with severe crescentic and necrotizing glomerulonephritis. Notably, only glomeruli with disrupted Bowman's capsule displayed massive CD8+ T cell infiltrates that were in direct contact with EGFP+ podocytes, causing their apoptosis. Thus, under control conditions with intact Bowman's capsule, podocytes are not accessible to CD8+ T cells. However, breaches in Bowman's capsule, as also noted in human crescentic glomerulonephritis, allow access of CD8+ T cells to the glomerular tuft and podocytes, resulting in their destruction. Through these mechanisms, a potentially reversible glomerulonephritis undergoes an augmentation process to a rapidly progressive glomerulonephritis, leading to end-stage kidney disease. Translating these mechanistic insights to human crescentic nephritis should direct future therapeutic interventions at blocking CD8+ T cells, especially in progressive stages of rapidly progressive glomerulonephritis.

Indexed as

AnimalsBowman CapsuleCD8-Positive T-LymphocytesGlomerulonephritisKidney Failure, ChronicMiceMice, TransgenicPodocytesChronic kidney diseaseImmunologyNephrologyT cells

Identifiers

PMID29985168
PMCPMC6063505
OpenAlexW2854095606

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.