Detection of anti‐D in D– recipients transfused with D+ red blood cells

Yazer, Mark H.; Triulzi, Darrell J.

doi:10.1111/j.1537-2995.2007.01446.x

Cited by 122 publications

(115 citation statements)

References 18 publications

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“…Alloimmunization to the RhD antigen on RBCs ranges from 20% to 80%, with only 3% to 10% of recipients becoming immunized to the remaining RBC antigens (eg, Kell, Duffy, Kidd), despite chronic transfusion. [3][4][5] The reason why some transfused patients but not others become alloimmunized is unclear, and factors influencing alloimmunization have been only partially defined. Immunogenetics plays some role in variability of alloimmunization to blood products, as antibody responses to certain alloantigens are confined to distinct recipient human leukocyte antigen (HLA) types.…”

Section: Introductionmentioning

confidence: 99%

Regulation of primary alloantibody response through antecedent exposure to a microbial T-cell epitope

Hudson

Lin

Hendrickson

et al. 2010

Blood

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Humoral alloimmunization to red blood cell (RBC) antigens is a clinically significant problem that can lead to transfusion reactions and difficulty in locating future compatible blood for transfusion. However, factors regulating responder/ nonresponder status are only partially understood. Herein, we identify a series of microbes with 100% identity in 8-to 9-amino acid peptides containing the variant amino acids in Kell, Kidd, and Duffy antigens. To test the hypothesis that infection with such a microbe could predispose to RBC alloimmunization, a mouse model was developed using murine polyoma virus expressing a defined CD4 ؉ Tcell epitope ovalbumin [323][324][325][326][327][328][329][330][331][332][333][334][335][336][337][338][339] IntroductionHumoral immunization to red blood cell (RBC) alloantigens can occur as a result of transfusion or pregnancy. Antibodies against clinically significant blood group alloantigens (ie, RhD, Kell, Kidd, etc) can lead to both hemolysis of transfused RBCs and/or to hemolytic disease of the newborn. 1,2 However, unlike humoral immunization to microbial infection, which approaches 100% in immunocompetent persons, exposure to RBC alloantigens induces a measurable antibody response in only a subset of recipients. Alloimmunization to the RhD antigen on RBCs ranges from 20% to 80%, with only 3% to 10% of recipients becoming immunized to the remaining RBC antigens (eg, Kell, Duffy, Kidd), despite chronic transfusion. [3][4][5] The reason why some transfused patients but not others become alloimmunized is unclear, and factors influencing alloimmunization have been only partially defined. Immunogenetics plays some role in variability of alloimmunization to blood products, as antibody responses to certain alloantigens are confined to distinct recipient human leukocyte antigen (HLA) types. [6][7][8] In addition, genetic variants outside of HLA may regulate RBC alloimmunization. 9 Environmental differences between recipients also likely affect alloimmunization, as genetically identical animals still have variable alloantibody responses to transfused RBCs. 10,11 One such environmental variable may be the inflammatory status of the recipient, which has been shown to have a substantial effect upon alloimmunization to transfused RBCs in mice, 10,12,13 and potentially in humans. 14 In the current report, we hypothesize that an additional potential factor is small peptide homology between microbial-derived peptides and blood group antigens.It has long been appreciated that alloimmunity can be induced through exposure to microbial antigens that mimic the 3-dimensional structure and epitopes of alloantigens (molecular mimicry); thus, antibodies generated against the microbial antigen can cross-react with alloantigens. This is a well-documented event with anti-ABO antibodies, where humans make antibodies against "non-self-" ABO antigens without any prior exposure through transfusion, because of immunization with gut microbes that express A and/or B antigens. 15 In the context of immunoglobulin G (...

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Section: Introductionmentioning

confidence: 99%

Regulation of primary alloantibody response through antecedent exposure to a microbial T-cell epitope

Hudson

Lin

Hendrickson

et al. 2010

Blood

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“…Because an immunization of more than 50% is not acceptable, measures to prevent exposure of patients negative for this Ag are taken whenever possible. Interestingly, studies have shown a high variability in the rate of immunization against RH1, suggesting the involvement of other factors [1,2]. A series of observations of transfused patients revealed the potential of immunization being associated with other RBC Ags; about 20 polymorphic molecules have the capacity of immunizing a significant number of recipients (but always less than 10%, which is the case for KEL1, RH3, RH4, JK1 and FY1, for others the rate is lower than 1% [3,4]), while the remaining 300 are have not been included in the statistics.…”

Section: The Immunogenicity Of Foreign Agsmentioning

confidence: 99%

From Donor to Recipient: Current Questions Relating to Humoral Alloimmunization

et al. 2014

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Alloimmunization is an undesirable iatrogenic effect of transfusion and transplantation. In fact, recipients can be considered as responders or not responders, in a continuum from tolerance, including organ transplantation and transfusion, to polyimmunized and refractory patients. New models and large studies have enabled a better understanding of the mechanisms that induce specific alloantibody (alloAb) generation. Here, we focus on risk factors of alloimmunization. We review the alloantibody characteristics, summarize the different leukocytes involved in their induction, and suggest some hypotheses.

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“…Thus, the incidence of alloimmunization has been widely cited as 80% primarily based on studies of healthy volunteers. Two more recent retrospective analyses of patients who received D2 mismatched transfusions indicate lower rates of alloimmunization, i.e., 16 of 78 (21%) transfused patients [6] and 22 of 98 (22%) nononcological transfused patients [7].…”

Section: Introductionmentioning

confidence: 99%

Prevention of Rh sensitization in the context of trauma: Two case reports

Werch

2009

J of Clinical Apheresis

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Background: Transfusion of D1 red blood cells (RBCs) to D2 recipients can be accidental or necessary due to D2 RBC shortage. Alloimmunization can complicate future transfusions; implications for women of childbearing age are compounded by possible hemolytic disease of the fetus and newborn. Rh immunoprophylaxis is effective, and indicated, for preventing alloimmunization. Reports of massive D1 mismatch (e.g., in the case of fetalmaternal bleed) are limited, and standard recommendations for managing these rare events are lacking. The cases discussed herein of women of childbearing age who suffered severe trauma requiring emergency surgery illustrate the dilemma of determining the ideal strategy for Rh immunoprophylaxis. Case reports: The first patient received two units of mismatched RBCs and was treated with intravenous Rh immune globulin (IV RHIG; Rhophylac 1 , CSL Behring, Kankakee, IL) monotherapy beginning 49 h postsurgery. For the second patient, who received three units of D1 RBCs, partial RBC exchange transfusion, followed 48 h later by IV RHIG, was deemed appropriate based on the large volume of RHIG needed and concerns of hemolytic transfusion reaction and hyperbilirubinemia. Both patients recovered in full without further intervention; the first patient delivered a healthy child 11 months posttreatment. Conclusions: Rh immunoprophylaxis is effective, and indicated, for preventing alloimmunization in women of childbearing age to protect the mother, fetus, and newborn.

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Detection of anti‐D in D– recipients transfused with D+ red blood cells

Abstract: The 22 percent rate of anti-D alloimmunization in patients requiring urgent RBC transfusion was intermediate between the rates previously reported for D- oncology patients transfused with D+ RBCs and that in immunocompetent volunteer recipients.

Cited by 122 publications

References 18 publications

Regulation of primary alloantibody response through antecedent exposure to a microbial T-cell epitope

Regulation of primary alloantibody response through antecedent exposure to a microbial T-cell epitope

From Donor to Recipient: Current Questions Relating to Humoral Alloimmunization

Prevention of Rh sensitization in the context of trauma: Two case reports

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