Evidence map›Paper›PMID 24708533›Full record

ArticleAmerican journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons2014

Characterization of transfusion-elicited acute antibody-mediated rejection in a rat model of kidney transplantation.

G Huang, N A Wilson, S R Reese, L M Jacobson, W Zhong, A Djamali

Open access · bronzeAbstract 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, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  18. Frontiers in immunology · 2017
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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

6 authors at 1 institution in 1 country.

G HuangDivision of Transplantation, Department of Surgery, University of Wisconsin School of Medicine and Public Health, Madison, WI.
N A Wilson
S R Reese
L M Jacobson
W Zhong
A Djamali
University of Wisconsin–Madison · US

Funding

WNPRC Supplemental Request for Nonhuman Primate Enclosures to Equip HIV/AIDS-Related Research FacilitiesP51OD011106 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI Dorota A. Grejner-Brzezinska · 2012 to 2026
$150.7M
ZOLEDRONATE PREVENTS BONE LOSS IN OVARIECTOMIZED RHESUS MONKEYSP51RR000167 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI WATKINS, DAVID I · 1985 to 2011
$106.7M
The role of Nox2 in CNI-induced renal fibrosisR01DK092454 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI DJAMALI, ARJANG · 2011 to 2015
$1.7M
NCRR NIH HHS P51 RR000167NIDDK NIH HHS R01 DK092454NIH HHS P51 OD011106
6 · The paper itself

Abstract

Animal models of antibody-mediated rejection (ABMR) may provide important evidence supporting proof of concept. We elicited donor-specific antibodies (DSA) by transfusion of donor blood (Brown Norway RT1(n) ) into a complete mismatch recipient (Lewis RT1(l) ) 3 weeks prior to kidney transplantation. Sensitized recipients had increased anti-donor splenocyte IgG1, IgG2b and IgG2c DSA 1 week after transplantation. Histopathology was consistent with ABMR characterized by diffuse peritubular capillary C4d and moderate microvascular inflammation with peritubular capillaritis + glomerulitis > 2. Immunofluorescence studies of kidney allograft tissue demonstrated a greater CD68/CD3 ratio in sensitized animals, primarily of the M1 (pro-inflammatory) phenotype, consistent with cytokine gene analyses that demonstrated a predominant T helper (TH )1 (interferon-γ, IL-2) profile. Immunoblot analyses confirmed the activation of the M1 macrophage phenotype as interferon regulatory factor 5, inducible nitric oxide synthase and phagocytic NADPH oxidase 2 were significantly up-regulated. Clinical biopsy samples in sensitized patients with acute ABMR confirmed the dominance of M1 macrophage phenotype in humans. Despite the absence of tubulitis, we were unable to exclude the effects of T cell-mediated rejection. These studies suggest that M1 macrophages and TH 1 cytokines play an important role in the pathogenesis of acute mixed rejection in sensitized allograft recipients.

Indexed as

Disease Models, AnimalKidney TransplantationTransfusion ReactionAnimalsBlotting, WesternComplement C4bCytokinesGraft RejectionHumansInflammationIsoantibodiesMalePeptide FragmentsRatsRats, Inbred BNRats, Inbred LewComplement C4bcomplement C4dCytokinesIsoantibodiesPeptide FragmentsRNA, MessengerAnimal modelantibody-mediated rejectionC4ddonor-specific antibodyphenotypetransfusion

Identifiers

PMID24708533
PMCPMC4289595
OpenAlexW1726106259

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.