Evidence map›Paper›PMID 23621760›Full record

ArticleTransfusion2014

Transfusion of murine red blood cells expressing the human KEL glycoprotein induces clinically significant alloantibodies.

Sean R Stowell, Kathryn R Girard-Pierce, Nicole H Smith, Kate L Henry, C Maridith Arthur, James C Zimring, Jeanne E Hendrickson

Abstract read
In one paragraph

Article in Transfusion, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 55 citations in OpenAlex.

  1. Acute Incompatible Red Blood Cell Transfusion in Mice.Methods in molecular biology (Clifton, N.J.) · 2026
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  3. The Immunology of Transfusion Medicine: Past, Present, and Future.Methods in molecular biology (Clifton, N.J.) · 2026
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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

7 authors at 4 institutions in 1 country.

Sean R StowellDepartment of Pathology, Emory University, Atlanta, Georgia; Aflac Cancer and Blood Disorders Center, Department of Pediatrics, Emory University, Atlanta, Georgia; Puget Sound Blood Center Research Institute, Seattle, Washington.
Kathryn R Girard-Pierce
Nicole H Smith
Kate L Henry
C Maridith Arthur
James C Zimring
Jeanne E Hendrickson
University Cancer and Blood Center · USCenter for Cancer and Blood Disorders · USBloodworks Northwest · USEmory University · US

Funding

Serious Hazards of Transfusion & Cellular Therapies: Mechanisms and InterventionP01HL086773 · NHLBI · EMORY UNIVERSITY · PI ROBACK, JOHN D · 2008 to 2019
$17.9M
Regulation of RBC Alloimmunization by Different Types of Recipient InflammationK08HL092959 · NHLBI · EMORY UNIVERSITY · PI HENDRICKSON, JEANNE E · 2009 to 2012
$514k
Immunoprophylaxis to Kell RBC Alloimmunization During PregnancyR21HL114696 · NHLBI · YALE UNIVERSITY · PI HENDRICKSON, JEANNE E · 2012 to 2013
$420k
NHLBI NIH HHS K08 HL092959NHLBI NIH HHS K08 HL092959,NHLBI NIH HHS P01 HL086773NHLBI NIH HHS R21 HL114696NHLBI NIH HHS R21 HL115696
6 · The paper itself

Abstract

backgroundRed blood cell (RBC) alloantibodies to nonself antigens may develop after transfusion or pregnancy, leading to morbidity and mortality in the form of hemolytic transfusion reactions or hemolytic disease of the newborn. A better understanding of the mechanisms of RBC alloantibody induction, or strategies to mitigate the consequences of such antibodies, may ultimately improve transfusion safety. However, such studies are inherently difficult in humans. STUDY DESIGN AND

methodsWe recently generated transgenic mice with RBC-specific expression of the human KEL glycoprotein, specifically the KEL2 or KEL1 antigens. Herein, we investigate recipient alloimmune responses to transfused RBCs in this system.

resultsTransfusion of RBCs from KEL2 donors into wild-type recipients (lacking the human KEL protein but expressing the murine KEL ortholog) resulted in dose-dependent anti-KEL glycoprotein immunoglobulin (Ig)M and IgG antibody responses, enhanced by recipient inflammation with poly(I:C). Boostable responses were evident upon repeat transfusion, with morbid-appearing alloimmunized recipients experiencing rapid clearance of transfused KEL2 but not control RBCs. Although KEL1 RBCs were also immunogenic after transfusion into wild-type recipients, transfusion of KEL1 RBCs into KEL2 recipients or vice versa failed to lead to detectable anti-KEL1 or anti-KEL2 responses.

conclusionsThis murine model, with reproducible and clinically significant KEL glycoprotein alloantibody responses, provides a platform for future mechanistic studies of RBC alloantibody induction and consequences. Long-term translational goals of these studies include improving transfusion safety for at-risk patients.

Indexed as

Anemia, HemolyticAnimalsAntibody FormationBlood Group IncompatibilityErythrocytesErythrocyte TransfusionHumansInflammationIsoantibodiesKell Blood-Group SystemMiceMice, Inbred C57BLMice, TransgenicPoly I-CIsoantibodiesKell Blood-Group SystemPoly I-C

Identifiers

PMID23621760
PMCPMC3732531
OpenAlexW1938446032

What OpenQuestion holds

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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.