Evidence map›Paper›PMID 35643350›Full record

ArticleTransplantation and cellular therapy2022

Mannan-Binding Lectin Promotes Murine Graft-versus-Host Disease by Amplifying Lipopolysaccharide-Initiated Inflammation.

David Heja, Dongchang Zhao, Evan Cody, Arun Cumpelik, Pik Chin Lim, Mariano Prado-Acosta, Liv Palma, Sergio Dellepiane, Nicholas Chun, James Ferrara and 1 more

Open access · greenAbstract read
In one paragraph

Article in Transplantation and cellular therapy, 2022. 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
0.1field-weighted citation impact, top 62% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

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 at 1 institution in 1 country.

David HejaTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Dongchang ZhaoTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Evan CodyTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Arun CumpelikTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Pik Chin LimTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Mariano Prado-AcostaTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Liv PalmaTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Sergio DellepianeTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Nicholas ChunTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
James FerraraTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Peter S HeegerTranslational Transplant Research Center, Tisch Cancer Institute, Precision Immunology Institute, Tisch Cancer Institute and Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: peter.heeger@mssm.edu.
Tisch Hospital · US

Funding

TUMOR VACCINES AND BONE MARROW TRANSPLANTATIONP01CA039542 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JAMES L. M. FERRARA · 1985 to 2026
$47.9M
Translational Immunology Training ProgramT32AI078892 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Karen Leigh Edelblum, SERGIO A. LIRA · 2008 to 2026
$4.5M
Cell Death Pathways and Heart Transplant RejectionR01AI132405 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HEEGER, PETER SCOTT, TING, ADRIAN T · 2017 to 2021
$2.8M
Complement Dependent Inflammation and Murine Heart Transplant RejectionK08AI135101 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHUN, NICHOLAS · 2018 to 2022
$951k
NCI NIH HHS P01 CA039542NIAID NIH HHS K08 AI135101NIAID NIH HHS R01 AI132405NIAID NIH HHS T32 AI078892
6 · The paper itself

Abstract

Conditioning regimens used for hematopoietic stem cell transplantation (HCT) can escalate the severity of acute T cell-mediated graft-versus-host disease (GVHD) by disrupting gastrointestinal integrity and initiating lipopolysaccharide (LPS)-dependent innate immune cell activation. Activation of the complement cascade has been associated with murine GVHD, and previous work has shown that alternative pathway complement activation can amplify T cell immunity. Whether and how mannan-binding lectin (MBL), a component of the complement system that binds mannose as well as oligosaccharide components of LPS and lipoteichoic acid, affects GVHD is unknown. In this study, we tested the hypothesis that MBL modulates murine GVHD and examined the mechanisms by which it does so. We adoptively transferred C3.SW bone marrow (BM) cells ± T cells into irradiated wild type (WT) or MBL-deficient C57Bl/6 (B6) recipients with or without inhibiting MBL-initiated complement activation using C1-esterase inhibitor (C1-INH). We analyzed the clinical severity of disease expression and analyzed intestinal gene and cell infiltration. In vitro studies assessed MBL expression on antigen-presenting cells (APCs) and compared LPS-induced responses of WT and MBL-deficient APCs. MBL-deficient recipients of donor BM ± T cells exhibited significantly less weight loss over the first 2 weeks post-transplantation weeks compared with B6 controls (P < .05), with similar donor engraftment in the 2 groups. In recipients of C3.SW BM + T cells, the clinical expression of GVHD was less severe (P < .05) and overall survival was better (P < .05) in MBL-deficient mice compared with WT mice. On day-7 post-transplantation, analyses showed that the MBL-deficient recipients exhibited less intestinal IL1b, IL17, and IL12 p40 gene expression (P < .05 for each) and fewer infiltrating intestinal CD11c

Indexed as

Graft vs Host DiseaseInflammationMannose-Binding LectinAnimalsBone Marrow TransplantationCD8-Positive T-LymphocytesLipopolysaccharidesMiceMice, Inbred C57BLTransplantation, HomologousLipopolysaccharidesMannose-Binding Lectinmannose binding protein AAcute GVHDComplementLPSMannan-binding lectin

Identifiers

PMID35643350
PMCPMC9357100
OpenAlexW4281481701

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.