Antibodies against biotin‐labeled red blood cells can shorten posttransfusion survival
Background In hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use of biotin‐labeled RBC (BioRBC) to determine red cell survival (RCS) offers substantial advantages over 51Cr and other labeling meth...
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| Published in | Transfusion (Philadelphia, Pa.) Vol. 62; no. 4; pp. 770 - 782 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken, USA
John Wiley & Sons, Inc
01.04.2022
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background
In hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use of biotin‐labeled RBC (BioRBC) to determine red cell survival (RCS) offers substantial advantages over 51Cr and other labeling methods. Occasional induction of BioRBC antibodies has been reported.
Study Design and Methods
To investigate the causes and consequences of BioRBC immunization, we reexposed three previously immunized adults to BioRBC and evaluated the safety, antibody emergence, and RCS of BioRBC.
Results
BioRBC re‐exposure caused an anamnestic increase of plasma BioRBC antibodies at 5–7 days; all were subclass IgG1 and neutralized by biotinylated albumin, thus indicating structural specificity for the biotin epitope. Concurrently, specific antibody binding to BioRBC was observed in each subject. As biotin label density increased, the proportion of BioRBC that bound increased antibody also increased; the latter was associated with proportional accelerated removal of BioRBC labeled at density 6 μg/mL. In contrast, only one of three subjects exhibited accelerated removal of BioRBC density 2 μg/mL. No adverse clinical or laboratory events were observed. Among three control subjects who did not develop BioRBC antibodies following initial BioRBC exposure, re‐exposure induced neither antibody emergence nor accelerated BioRBC removal.
Discussion
We conclude re‐exposure of immunized subjects to BioRBC can induce anamnestic antibody response that can cause an underestimation of RCS. To minimize chances of antibody induction and underestimation of RCS, we recommend an initial BioRBC exposure volume of ≤10 mL and label densities of ≤18 μg/mL. |
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| AbstractList | In hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use of biotin-labeled RBC (BioRBC) to determine red cell survival (RCS) offers substantial advantages over 51 Cr and other labeling methods. Occasional induction of BioRBC antibodies has been reported.BACKGROUNDIn hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use of biotin-labeled RBC (BioRBC) to determine red cell survival (RCS) offers substantial advantages over 51 Cr and other labeling methods. Occasional induction of BioRBC antibodies has been reported.To investigate the causes and consequences of BioRBC immunization, we reexposed three previously immunized adults to BioRBC and evaluated the safety, antibody emergence, and RCS of BioRBC.STUDY DESIGN AND METHODSTo investigate the causes and consequences of BioRBC immunization, we reexposed three previously immunized adults to BioRBC and evaluated the safety, antibody emergence, and RCS of BioRBC.BioRBC re-exposure caused an anamnestic increase of plasma BioRBC antibodies at 5-7 days; all were subclass IgG1 and neutralized by biotinylated albumin, thus indicating structural specificity for the biotin epitope. Concurrently, specific antibody binding to BioRBC was observed in each subject. As biotin label density increased, the proportion of BioRBC that bound increased antibody also increased; the latter was associated with proportional accelerated removal of BioRBC labeled at density 6 μg/mL. In contrast, only one of three subjects exhibited accelerated removal of BioRBC density 2 μg/mL. No adverse clinical or laboratory events were observed. Among three control subjects who did not develop BioRBC antibodies following initial BioRBC exposure, re-exposure induced neither antibody emergence nor accelerated BioRBC removal.RESULTSBioRBC re-exposure caused an anamnestic increase of plasma BioRBC antibodies at 5-7 days; all were subclass IgG1 and neutralized by biotinylated albumin, thus indicating structural specificity for the biotin epitope. Concurrently, specific antibody binding to BioRBC was observed in each subject. As biotin label density increased, the proportion of BioRBC that bound increased antibody also increased; the latter was associated with proportional accelerated removal of BioRBC labeled at density 6 μg/mL. In contrast, only one of three subjects exhibited accelerated removal of BioRBC density 2 μg/mL. No adverse clinical or laboratory events were observed. Among three control subjects who did not develop BioRBC antibodies following initial BioRBC exposure, re-exposure induced neither antibody emergence nor accelerated BioRBC removal.We conclude re-exposure of immunized subjects to BioRBC can induce anamnestic antibody response that can cause an underestimation of RCS. To minimize chances of antibody induction and underestimation of RCS, we recommend an initial BioRBC exposure volume of ≤10 mL and label densities of ≤18 μg/mL.DISCUSSIONWe conclude re-exposure of immunized subjects to BioRBC can induce anamnestic antibody response that can cause an underestimation of RCS. To minimize chances of antibody induction and underestimation of RCS, we recommend an initial BioRBC exposure volume of ≤10 mL and label densities of ≤18 μg/mL. Background In hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use of biotin‐labeled RBC (BioRBC) to determine red cell survival (RCS) offers substantial advantages over 51Cr and other labeling methods. Occasional induction of BioRBC antibodies has been reported. Study Design and Methods To investigate the causes and consequences of BioRBC immunization, we reexposed three previously immunized adults to BioRBC and evaluated the safety, antibody emergence, and RCS of BioRBC. Results BioRBC re‐exposure caused an anamnestic increase of plasma BioRBC antibodies at 5–7 days; all were subclass IgG1 and neutralized by biotinylated albumin, thus indicating structural specificity for the biotin epitope. Concurrently, specific antibody binding to BioRBC was observed in each subject. As biotin label density increased, the proportion of BioRBC that bound increased antibody also increased; the latter was associated with proportional accelerated removal of BioRBC labeled at density 6 μg/mL. In contrast, only one of three subjects exhibited accelerated removal of BioRBC density 2 μg/mL. No adverse clinical or laboratory events were observed. Among three control subjects who did not develop BioRBC antibodies following initial BioRBC exposure, re‐exposure induced neither antibody emergence nor accelerated BioRBC removal. Discussion We conclude re‐exposure of immunized subjects to BioRBC can induce anamnestic antibody response that can cause an underestimation of RCS. To minimize chances of antibody induction and underestimation of RCS, we recommend an initial BioRBC exposure volume of ≤10 mL and label densities of ≤18 μg/mL. BackgroundIn hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use of biotin‐labeled RBC (BioRBC) to determine red cell survival (RCS) offers substantial advantages over 51Cr and other labeling methods. Occasional induction of BioRBC antibodies has been reported.Study Design and MethodsTo investigate the causes and consequences of BioRBC immunization, we reexposed three previously immunized adults to BioRBC and evaluated the safety, antibody emergence, and RCS of BioRBC.ResultsBioRBC re‐exposure caused an anamnestic increase of plasma BioRBC antibodies at 5–7 days; all were subclass IgG1 and neutralized by biotinylated albumin, thus indicating structural specificity for the biotin epitope. Concurrently, specific antibody binding to BioRBC was observed in each subject. As biotin label density increased, the proportion of BioRBC that bound increased antibody also increased; the latter was associated with proportional accelerated removal of BioRBC labeled at density 6 μg/mL. In contrast, only one of three subjects exhibited accelerated removal of BioRBC density 2 μg/mL. No adverse clinical or laboratory events were observed. Among three control subjects who did not develop BioRBC antibodies following initial BioRBC exposure, re‐exposure induced neither antibody emergence nor accelerated BioRBC removal.DiscussionWe conclude re‐exposure of immunized subjects to BioRBC can induce anamnestic antibody response that can cause an underestimation of RCS. To minimize chances of antibody induction and underestimation of RCS, we recommend an initial BioRBC exposure volume of ≤10 mL and label densities of ≤18 μg/mL. In hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use of biotin-labeled RBC (BioRBC) to determine red cell survival (RCS) offers substantial advantages over Cr and other labeling methods. Occasional induction of BioRBC antibodies has been reported. To investigate the causes and consequences of BioRBC immunization, we reexposed three previously immunized adults to BioRBC and evaluated the safety, antibody emergence, and RCS of BioRBC. BioRBC re-exposure caused an anamnestic increase of plasma BioRBC antibodies at 5-7 days; all were subclass IgG and neutralized by biotinylated albumin, thus indicating structural specificity for the biotin epitope. Concurrently, specific antibody binding to BioRBC was observed in each subject. As biotin label density increased, the proportion of BioRBC that bound increased antibody also increased; the latter was associated with proportional accelerated removal of BioRBC labeled at density 6 μg/mL. In contrast, only one of three subjects exhibited accelerated removal of BioRBC density 2 μg/mL. No adverse clinical or laboratory events were observed. Among three control subjects who did not develop BioRBC antibodies following initial BioRBC exposure, re-exposure induced neither antibody emergence nor accelerated BioRBC removal. We conclude re-exposure of immunized subjects to BioRBC can induce anamnestic antibody response that can cause an underestimation of RCS. To minimize chances of antibody induction and underestimation of RCS, we recommend an initial BioRBC exposure volume of ≤10 mL and label densities of ≤18 μg/mL. |
| Author | Cress, Gretchen A. North, Anne K. Strauss, Ronald G. Mock, Donald M. Kyosseva, Svetlana V. Widness, John A. Stowell, Sean R. Goetz, Melissa Schmidt, Robert L. Franco, Robert S. Cancelas, José A. Nalbant, Demet |
| AuthorAffiliation | 3 Division of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA 4 Department of Pharmaceutical Sciences and Experimental Therapeutics, University of Iowa College of Pharmacy, Iowa City, Iowa, USA 5 Stead Family Department of Pediatrics, The University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa, USA 2 Center for Transfusion and Cellular Therapies, Departments of Pathology and Laboratory Medicine and Pediatrics, Emory University School of Medicine, Atlanta, Georgia, USA 8 Cerus Corporation, Concord, California, USA 6 Department of Pathology, The University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa, USA 7 Hoxworth Blood Center and Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio, USA 1 Department of Biochemistry & Molecular Biology and the Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA |
| AuthorAffiliation_xml | – name: 6 Department of Pathology, The University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa, USA – name: 7 Hoxworth Blood Center and Department of Pediatrics, University of Cincinnati, Cincinnati, Ohio, USA – name: 3 Division of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA – name: 4 Department of Pharmaceutical Sciences and Experimental Therapeutics, University of Iowa College of Pharmacy, Iowa City, Iowa, USA – name: 5 Stead Family Department of Pediatrics, The University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa, USA – name: 8 Cerus Corporation, Concord, California, USA – name: 2 Center for Transfusion and Cellular Therapies, Departments of Pathology and Laboratory Medicine and Pediatrics, Emory University School of Medicine, Atlanta, Georgia, USA – name: 1 Department of Biochemistry & Molecular Biology and the Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA |
| Author_xml | – sequence: 1 givenname: Donald M. surname: Mock fullname: Mock, Donald M. email: mockdonaldm@uams.edu organization: University of Arkansas for Medical Sciences – sequence: 2 givenname: Sean R. orcidid: 0000-0002-1130-9551 surname: Stowell fullname: Stowell, Sean R. organization: Emory University School of Medicine – sequence: 3 givenname: Robert S. surname: Franco fullname: Franco, Robert S. organization: University of Cincinnati College of Medicine – sequence: 4 givenname: Svetlana V. surname: Kyosseva fullname: Kyosseva, Svetlana V. organization: University of Arkansas for Medical Sciences – sequence: 5 givenname: Demet surname: Nalbant fullname: Nalbant, Demet organization: University of Iowa College of Pharmacy – sequence: 6 givenname: Robert L. surname: Schmidt fullname: Schmidt, Robert L. organization: The University of Iowa, Roy J. and Lucille A. Carver College of Medicine – sequence: 7 givenname: Gretchen A. surname: Cress fullname: Cress, Gretchen A. organization: The University of Iowa, Roy J. and Lucille A. Carver College of Medicine – sequence: 8 givenname: Ronald G. surname: Strauss fullname: Strauss, Ronald G. organization: The University of Iowa, Roy J. and Lucille A. Carver College of Medicine – sequence: 9 givenname: José A. surname: Cancelas fullname: Cancelas, José A. organization: University of Cincinnati – sequence: 10 givenname: Melissa surname: Goetz fullname: Goetz, Melissa organization: Cerus Corporation – sequence: 11 givenname: Anne K. surname: North fullname: North, Anne K. organization: Cerus Corporation – sequence: 12 givenname: John A. orcidid: 0000-0001-6543-5927 surname: Widness fullname: Widness, John A. organization: The University of Iowa, Roy J. and Lucille A. Carver College of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35274303$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3390_bios13010117 crossref_primary_10_1111_trf_17033 crossref_primary_10_1016_j_humimm_2024_111084 crossref_primary_10_1097_MOH_0000000000000783 crossref_primary_10_1016_j_tmrv_2023_01_001 crossref_primary_10_1111_trf_17800 crossref_primary_10_1146_annurev_pathol_042320_110411 crossref_primary_10_3389_fmicb_2024_1348873 crossref_primary_10_1016_j_tmrv_2023_150758 |
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| Keywords | biotin-labeled RBC BioRBC antibodies RBC posttransfusion kinetics biotin |
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| Notes | Funding information The sponsors of this work had no role in this work including: study design; the collection, analysis, and interpretation of data; the writing of the report; and the decision to submit the manuscript for publication. The sponsors of this work include: The United States Public Health Service National Institutes of Health Grants P01 HL046925 and R01 DK063088 (RSF); The Thrasher Research Fund 0285‐3; The National Center for Research Resources, a part of the National Institutes of Health (NIH) CTSA Grants U54TR001356 (U Iowa), UL1TR000039/U54TR001629/UL1TR003107 (UAMS Translational Research Institute), and 1S10 RR027219, and UL1 TR001425 (University of Cincinnati). Some of the flow cytometry data were obtained at the Flow Cytometry Facility, which is a core research facility at the University of Arkansas for Medical Sciences; support was also provided by the NHLBI Summer Undergraduate Research Program to Increase Diversity in Research (SURP grant) R25 HL108825 (UAMS). Some of the flow cytometry data were obtained at the Flow Cytometry Facility, which is a Carver College of Medicine/Holden Comprehensive Cancer Center core research facility at the University of Iowa. The facility is funded through user fees and the generous financial support of the Carver College of Medicine, Holden Comprehensive Cancer Center, and Iowa City Veteran's Administration Medical Center. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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In hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports... In hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports indicate use... BackgroundIn hematologic and transfusion medicine research, measurement of red blood cell (RBC) in vivo kinetics must be safe and accurate. Recent reports... |
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| SubjectTerms | Adult Albumins Antibodies Antibodies - metabolism Antibody response BioRBC antibodies Biotin Biotin - chemistry biotin‐labeled RBC Cell Survival Chromium radioisotopes Density Epitopes Erythrocyte Count Erythrocytes Erythrocytes - metabolism Exposure Humans Immunization Immunoglobulin G RBC posttransfusion kinetics Survival Transfusion |
| Title | Antibodies against biotin‐labeled red blood cells can shorten posttransfusion survival |
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