Purpose of review: To discuss how inflammation affects humoral alloimmunization to antigens on transfused red blood cells (RBCs).
Recent findings: Recently, three unique murine models of humoral alloimmunization to transfused RBCs have been described. As in humans, RBC alloimmunization rates in recipient mice are variable, with segregation into responder and nonresponder groups. Because the recipient mice are genetically identical, environmental factors may play a role in regulating alloimmunization. These models have further been used to demonstrate that recipient inflammation has a complex regulatory effect upon alloimmunization. Isolated case reports in humans raise the possibility of a similar role of inflammation in regulating alloimmunization to RBCs.
Summary: It is currently unknown why some human transfusion recipients mount strong alloantibody responses, whereas others do not. Human leukocyte antigen immunogenetics likely play a substantial role. However, within groups with the genetic capacity to respond to a given RBC antigen, recipients still segregate into responders and nonresponders. The data reviewed herein indicate that recipient inflammation in mice has the capacity to regulate alloimmunization. Future studies will be required to further understand these effects and to investigate if similar biology regulates alloimmunization to transfused RBCs in humans.