Evidence map›Paper›PMID 40980674›Full record

ArticleKidney international reports2025

The Immune Microenvironment of Transplant Glomerulitis.

Nathan A Bracey, Jonathan S Maltzman, Adrienne H Long, Renu Dhanasekaran, Vishnu Shankar, Azam Mohsin, Neeraja Kambham, Gerlinde Wernig, Andrew J Gentles, Mark M Davis and 1 more

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Article in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Nathan A BraceyInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, California, USA.
Jonathan S MaltzmanDepartment of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Adrienne H LongInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, California, USA.
Renu DhanasekaranDivision of Gastroenterology and Hepatology, Stanford University, Stanford, California, USA.
Vishnu ShankarInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, California, USA.
Azam MohsinInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, California, USA.
Neeraja KambhamDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Gerlinde WernigDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Andrew J GentlesDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.
Mark M DavisInstitute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, California, USA.
Vivek CharuDepartment of Pathology, Stanford University School of Medicine, Stanford, California, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Transplant glomerulitis is a morphological lesion seen in kidney allograft rejection that is associated with poor outcomes; however, little is known about how immune cells infiltrate and organize specifically within glomeruli. Methods: We used Co-Detection by Indexing (CODEX) multifluorescent imaging to measure 52 protein markers in a retrospective cohort of 41 human allograft nephrectomies (ANs) and evaluated the immunological landscape of transplant glomerulitis. Results: Characterization of 18 cell types identified diverse immune cells within inflamed glomeruli, with unique phenotypes and compositions compared with the extraglomerular microenvironment. Immunological phenotypes were conserved across glomeruli within individuals and associated with the general state of injury, with M1 macrophages and effector CD8 T cells associated with mild inflammation. Distance-based spatial analysis further revealed a profibrotic community composed of M2 macrophages, memory CD8 T cells and exhausted CD8 T cells surrounding endothelial cell hubs. These interaction networks were associated with regions of adverse glomerular remodeling, expression of profibrotic proteins, and were more prevalent in individuals with C4d-positive rejection. Conclusion: These results implicate distinct cell-cell interactions as hallmarks of alloimmune injury and chronic remodeling during transplant glomerulitis and may give rise to new tools for histological risk assessment of clinical rejection syndromes.

Indexed as

cell-cell communicationkidney rejectionsingle-celltransplant glomerulitis

Identifiers

PMID40980674
PMCPMC12446868

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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.