Red blood cell alloimmunization: new findings at the bench and new recommendations for the bedside

Curr Opin Hematol. 2016 Nov;23(6):543-549. doi: 10.1097/MOH.0000000000000277.

Abstract

Purpose of review: To summarize recent discoveries from clinical studies and animal models that contribute to understanding the alloimmune response to non-ABO blood group antigens.

Recent findings: Several studies have confirmed high rates of alloimmunization among patients requiring chronic red blood cell (RBC) transfusion. Moreover, 'triggers' for alloantibody development in the transfusion setting have been identified, with a number of investigations linking recipient inflammation to a higher likelihood of alloimmunization. Additional associations between human leukocyte antigen expression and CD4 T-cell markers in 'responder' or 'nonresponder' humans have been revealed. Recent animal studies have described novel mechanistic properties by which the alloimmune response is governed, including the critical role played by dendritic cells in transfusion-associated alloimmunization. New light has also been shed on the properties of alloantibodies developed as a result of pregnancy, as well as mechanisms through which such alloimmunization may be prevented.

Summary: Many of the clinical/biological factors that contribute to the RBC alloimmune response have been further elucidated. This knowledge will be applied to identify individuals most likely to mount an immune response to RBC antigens, such that appropriate resources and strategies for preventing alloimmunization (or mitigating its harmful effects) can be implemented.

Publication types

  • Review

MeSH terms

  • Animals
  • Antigens / genetics
  • Antigens / immunology
  • Erythroblastosis, Fetal / diagnosis
  • Erythroblastosis, Fetal / etiology
  • Erythroblastosis, Fetal / prevention & control
  • Erythrocytes / immunology*
  • Humans
  • Immunization*
  • Isoantibodies / immunology*
  • Models, Animal
  • Research
  • Risk Factors
  • Seroepidemiologic Studies
  • Transfusion Reaction* / etiology

Substances

  • Antigens
  • Isoantibodies