Evidence map›Paper›PMID 33421294›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2021

Follicular T cells mediate donor-specific antibody and rejection after solid organ transplantation.

Mostafa T Mohammed, Songjie Cai, Benjamin L Hanson, Hengcheng Zhang, Rachel L Clement, Joe Daccache, Cecilia B Cavazzoni, Bruce R Blazar, Alessandro Alessandrini, Helmut G Rennke and 2 more

Open access · hybridAbstract read
In one paragraph

Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.5field-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

35 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. T cell senescence induced by DNMT1 deletion mediates cardiac transplant tolerance via altered CDKN1A methylation.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  5. Review
  6. Review
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  11. Progressively differentiated TNature immunology · 2025
    Article
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  14. Review
  15. Review
  16. Article
  17. Review
  18. Targeting THaematologica · 2024
    Article
  19. Article
  20. Article
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

12 authors at 3 institutions in 2 countries.

Mostafa T MohammedClinical Pathology Department, Faculty of Medicine, Minia University, Minia, Egypt.ORCID 0000-0002-6071-9602
Songjie CaiTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-8166-4356
Benjamin L HansonTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0003-3090-3270
Hengcheng ZhangTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-2562-1247
Rachel L ClementTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Joe DaccacheTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Cecilia B CavazzoniTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Bruce R BlazarDepartment of Pediatrics, Division of Blood and Marrow Transplantation, University of Minnesota, Minneapolis, Minnesota.
Alessandro AlessandriniCenter for Transplantation Sciences, Department of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Helmut G RennkeDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Anil ChandrakerTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0001-9729-7717
Peter T SageTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.ORCID 0000-0002-7287-0326
Brigham and Women's Hospital · USHarvard University · USUniversity of Minnesota · US

Funding

Trial Design and Biostatistical Support CoreP01CA065493 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI J SUNIL RAO · 1995 to 2026
$48.2M
Transgenic/KnockoutP01AI056299 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BLAZAR, BRUCE R · 2003 to 2023
$42.5M
Project 3: Humoral Targets and B Cell Biology in Chronic Graft-vs.-Host DiseaseP01CA142106 · NCI · DANA-FARBER CANCER INST · PI RITZ, JEROME · 2009 to 2019
$17.5M
Project 3: The Role of Erythropoietin in Kidney Transplant ToleranceP01AI123086 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI MADSEN, JOREN C · 2016 to 2020
$10.6M
In Vivo Prevention of Murine GVHDR37AI034495 · NIAID · UNIVERSITY OF MINNESOTA · PI Bruce R Blazar · 2017 to 2026
$5.4M
Nongenotoxic conditioning for gene therapy and allogeneic transplantation in Fanconi anemiaR01HL147324 · NHLBI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Bruce R Blazar, HANS-PETER KIEM · 2020 to 2026
$4.1M
Control of antibody responses in vaccination and allergic inflammation by follicular regulatory T cellsK22AI132937 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI SAGE, PETER THE · 2018 to 2019
$267k
NCI NIH HHS P01 CA065493NCI NIH HHS P01 CA142106NHLBI NIH HHS R01 HL147324NIAID NIH HHS K22 AI132937NIAID NIH HHS P01 AI056299NIAID NIH HHS P01 AI123086NIAID NIH HHS R37 AI034495
6 · The paper itself

Abstract

Following solid organ transplantation, a substantial proportion of chronic allograft loss is attributed to the formation of donor-specific antibodies (DSAs) and antibody-mediated rejection (AbMR). The frequency and phenotype of T follicular helper (Tfh) and T follicular regulatory (Tfr) cells is altered in the setting of kidney transplantation, particularly in patients who develop AbMR. However, the roles of Tfh and Tfr cells in AbMR after solid organ transplantation is unclear. We developed mouse models to inducibly and potently perturb Tfh and Tfr cells to assess the roles of these cells in the development of DSA and AbMR. We found that Tfh cells are required for both de novo DSA responses as well as augmentation of DSA following presensitization. Using orthotopic allogeneic kidney transplantation models, we found that deletion of Tfh cells at the time of transplantation resulted in less severe transplant rejection. Furthermore, using inducible Tfr cell deletion strategies we found that Tfr cells inhibit de novo DSA formation but only have a minor role in controlling kidney transplant rejection. These studies demonstrate that Tfh cells promote, whereas Tfr cells inhibit, DSA to control rejection after kidney transplantation. Therefore, targeting these cells represent a new therapeutic strategy to prevent and treat AbMR.

Indexed as

Kidney TransplantationOrgan TransplantationAnimalsAntibodiesGraft RejectionHumansMiceTissue DonorsAntibodiesalloantibodyanimal models: murinebasic (laboratory) research / scienceB cell biologyimmune regulationimmunosuppression / immune modulationkidney transplantation / nephrology

Identifiers

PMID33421294
PMCPMC8096660
OpenAlexW3120760716

What OpenQuestion holds

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Registered trials

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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.