Evidence map›Paper›PMID 35634722›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2022

Plasma CXCL9 and CXCL10 at allograft injury predict chronic lung allograft dysfunction.

Michael Y Shino, Jamie L Todd, Megan L Neely, Jerry Kirchner, Courtney W Frankel, Laurie D Snyder, Elizabeth N Pavlisko, Gregory A Fishbein, Joanna M Schaenman, Kristen Mason and 12 more

Registry-linked trialOpen access · bronzeAbstract readMulticenter Study
In one paragraph

Article in American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07538336 (Targeting Interferon Gamma With Emapalumab to Lung Transplant Recipients With Interferon Gamma-high Acute Lung Allograft Dysfunction), which is not on this map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.0field-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.

NCT07538336 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Targeting Interferon Gamma With Emapalumab to Lung Transplant Recipients With Interferon Gamma-high Acute Lung Allograft Dysfunction

TypeinterventionalSponsorUniversity of California, San FranciscoRan2026 to 2028Enrolled40ConditionsLung TransplantArmsEmapalumab, Placebo
3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. The importance of B cells for osteogenic homeostasis.Cell communication and signaling : CCS · 2026
    Article
  2. Donor-derived cell-free DNA associated with increased risk of chronic lung allograft dysfunction and mortality: Are absolute levels better than percentage?The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026
    Observational
  3. Article
  4. Article
  5. Article
  6. Persistent and progressive acute lung allograft dysfunction is linked to cell compositional and transcriptional changes in small airways.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Small airway brush gene expression predicts chronic lung allograft dysfunction and mortality.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2024
    Article
  12. Review
  13. Article
  14. Prognostic implications of and clinical risk factors for acute lung injury and organizing pneumonia after lung transplantation: Data from a multicenter prospective cohort study.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
    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

22 authors at 7 institutions in 2 countries.

Michael Y ShinoUniversity of California Los Angeles, Los Angeles, California, USA.ORCID 0000-0001-9261-1404
Jamie L ToddDuke University Medical Center, Durham, North Carolina, USA.ORCID 0000-0003-4247-3693
Megan L NeelyDuke University Medical Center, Durham, North Carolina, USA.
Jerry KirchnerDuke University Medical Center, Durham, North Carolina, USA.
Courtney W FrankelDuke University Medical Center, Durham, North Carolina, USA.
Laurie D SnyderDuke University Medical Center, Durham, North Carolina, USA.ORCID 0000-0002-5962-2184
Elizabeth N PavliskoDuke University Medical Center, Durham, North Carolina, USA.
Gregory A FishbeinUniversity of California Los Angeles, Los Angeles, California, USA.ORCID 0000-0002-3632-5654
Joanna M SchaenmanUniversity of California Los Angeles, Los Angeles, California, USA.ORCID 0000-0003-1174-3961
Kristen MasonRho, Durham, North Carolina, USA.
Karen KeslerRho, Durham, North Carolina, USA.
Tereza MartinuUniversity Health Network University of Toronto, Ontario, Canada.
Lianne G SingerUniversity Health Network University of Toronto, Ontario, Canada.ORCID 0000-0002-2693-8676
Wayne TsuangCleveland Clinic, Cleveland, Ohio, USA.ORCID 0000-0001-7375-3845
Marie BudevCleveland Clinic, Cleveland, Ohio, USA.
Pali D ShahJohn Hopkins University, Baltimore, Maryland, USA.
John M ReynoldsDuke University Medical Center, Durham, North Carolina, USA.
Nikki WilliamsNational Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA.
Mark A RobienNational Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA.
Scott M PalmerDuke University Medical Center, Durham, North Carolina, USA.ORCID 0000-0002-1370-3771
S Sam WeigtUniversity of California Los Angeles, Los Angeles, California, USA.
John A BelperioUniversity of California Los Angeles, Los Angeles, California, USA.
Duke Medical Center · USUniversity of California, Los Angeles · USCleveland Clinic · USNational Institute of Allergy and Infectious Diseases · USRho (United States) · USUniversity Health Network · CAJohns Hopkins University · US

Funding

Transplantation GroupUM2AI117870 · NIAID · RHO FEDERAL SYSTEMS DIVISION, INC. · PI DAVID, GLORIA · 2015 to 2023
$208.1M
Role of Surfactant Proteins in Mediating Noninfectious Inflammatory and FibroproP01HL108793 · NHLBI · DUKE UNIVERSITY · PI STRIPP, BARRY R · 2012 to 2022
$21.3M
The Lung Transplant Clinical Trials Network (LT-CTN)U01AI113315 · NIAID · DUKE UNIVERSITY · PI PALMER, SCOTT M · 2014 to 2018
$12.9M
UCLA Pulmonary and Critical Care Medicine Training ProgramT32HL072752 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JOHN A BELPERIO, TOMAS GANZ · 2003 to 2026
$8.3M
Immune Mechanisms of AlloinjuryR01HL112990 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BELPERIO, JOHN A · 2012 to 2016
$2.2M
Non-invasive surveillance of the lung allograft post transplantationK23HL138256 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHINO, YUSAKU MICHAEL · 2017 to 2021
$902k
NHLBI NIH HHS K23 HL138256NHLBI NIH HHS P01 HL108793NHLBI NIH HHS R01 HL112990NHLBI NIH HHS T32 HL072752NIAID NIH HHS U01 AI113315NIAID NIH HHS UM2 AI117870
6 · The paper itself

Abstract

Histopathologic lung allograft injuries are putative harbingers for chronic lung allograft dysfunction (CLAD). However, the mechanisms responsible are not well understood. CXCL9 and CXCL10 are potent chemoattractants of mononuclear cells and potential propagators of allograft injury. We hypothesized that these chemokines would be quantifiable in plasma, and would associate with subsequent CLAD development. In this prospective multicenter study, we evaluated 721 plasma samples for CXCL9/CXCL10 levels from 184 participants at the time of transbronchial biopsies during their first-year post-transplantation. We determined the association between plasma chemokines, histopathologic injury, and CLAD risk using Cox proportional hazards models. We also evaluated CXCL9/CXCL10 levels in bronchoalveolar lavage (BAL) fluid and compared plasma to BAL with respect to CLAD risk. Plasma CXCL9/CXCL10 levels were elevated during the injury patterns associated with CLAD, acute rejection, and acute lung injury, with a dose-response relationship between chemokine levels and CLAD risk. Importantly, there were strong interactions between injury and plasma CXCL9/CXCL10, where histopathologic injury associated with CLAD only in the presence of elevated plasma chemokines. We observed similar associations and interactions with BAL CXCL9/CXCL10 levels. Elevated plasma CXCL9/CXCL10 during allograft injury may contribute to CLAD pathogenesis and has potential as a minimally invasive immune monitoring biomarker.

Indexed as

Graft vs Host DiseaseLung TransplantationAllograftsBiomarkersChemokine CXCL10Chemokine CXCL9Graft RejectionHumansLungProspective StudiesBiomarkersChemokine CXCL10Chemokine CXCL9CXCL10 protein, humanCXCL9 protein, humancytokines/cytokine receptorsimmunobiologylung (allograft) function/dysfunctionlung failure/injurylung transplantation: living donorlung transplantation/pulmonologypathology/histopathologyrejection: acutetranslational research/science

Identifiers

PMID35634722
PMCPMC9427677
OpenAlexW4281627089

What OpenQuestion holds

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Registered trials

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.