Evidence map›Paper›PMID 33273321›Full record

ArticleTransplantation2021

B-cell Deficiency Attenuates Transplant Glomerulopathy in a Rat Model of Chronic Active Antibody-mediated Rejection.

Shannon R Reese, Nancy A Wilson, Yabing Huang, Lucille Ptak, Kenna R Degner, Ding Xiang, Robert R Redfield, Weixiong Zhong, Sarah E Panzer

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Transplantation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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

9 authors at 3 institutions in 2 countries.

Shannon R ReeseDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
Nancy A WilsonDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
Yabing HuangDepartment of Pathology, Renmin Hospital of Wuhan University, Wuchang District, Wuhan, China.
Lucille PtakDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
Kenna R DegnerDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
Ding XiangDepartment of Organ Transplantation, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Robert R RedfieldDivision of Transplant Surgery, Department of Surgery, University of Wisconsin, Madison, WI.
Weixiong ZhongDepartment of Pathology, University of Wisconsin, Madison, WI.
Sarah E PanzerDivision of Nephrology, Department of Medicine, University of Wisconsin, Madison, WI.
University of Wisconsin–Madison · USCentral South University · CNWuhan University · CN

Funding

University of Wisconsin Transplant Reseach Training ProgramT32AI125231 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI KAUFMAN, DIXON B · 2016 to 2020
$1.2M
Improving long-term allograft survival in kidney transplantation by targeting B cell survival cytokinesK23DK122136 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI PANZER, SARAH E · 2019 to 2022
$663k
NIAID NIH HHS T32 AI125231NIDDK NIH HHS K23 DK122136NIDDK NIH HHS L30 DK126100
6 · The paper itself

Abstract

backgroundTransplant glomerulopathy (TG) is a pathological feature of chronic active antibody-mediated rejection (cAMR) and is associated with renal allograft failure. The specific role of B cells in the pathogenesis of TG is unclear.

methodsWe used a minor mismatched rat kidney transplant model with B cell-deficient recipients, generated by clustered regularly interspaced short palindromic repeats/Cas9 technology, to investigate the impact of B-cell depletion on the pathogenesis of TG. We hypothesized that B-cell deficiency would prevent TG in the rat kidney transplant model of cAMR. Treatment groups included syngeneic, allogeneic, sensitized allogeneic, and B cell-deficient allogeneic transplant recipients.

resultsB cell-deficient recipients demonstrated reduced TG lesions, decreased microvascular inflammation, reduced allograft infiltrating macrophages, and reduced interferon gamma transcripts within the allograft. Allograft transcript levels of interferon gamma, monocyte chemoattractant protein-1, and interleukin-1β correlated with numbers of intragraft macrophages. B cell-deficient recipients lacked circulating donor-specific antibodies and had an increased splenic regulatory T-cell population.

conclusionsIn this model of cAMR, B-cell depletion attenuated the development of TG with effects on T cell and innate immunity.

Indexed as

AnimalsB-LymphocytesCell ProliferationCells, CulturedChronic DiseaseCoculture TechniquesCytokinesDisease Models, AnimalGlomerulonephritisGraft RejectionImmunity, CellularImmunity, InnateInflammation MediatorsIsoantibodiesKidneyLymphocyte ActivationCytokinesInflammation MediatorsIsoantibodies

Identifiers

PMID33273321
PMCPMC8106694
OpenAlexW3110416211

What OpenQuestion holds

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LicenceTDM
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.