Autoantibody formation after alloimmunization: are blood tranfusions a risk factor for autoimmune hemolytic anemia?

Young, Pampee P.; Uzieblo, Alison; Trulock, Elbert P.; Lublin, Doug M.; Goodnough, Lawrence T.

doi:10.1046/j.0041-1132.2003.00589.x

Cited by 98 publications

(95 citation statements)

References 29 publications

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“…About a third of them developed their autoantibody in close temporal association with alloimmunization following recent transfusion. 9 Therefore, AIHA developed either concurrently or shortly after alloimmunization from blood transfusion. The authors conclude that AIHA is a potential complication of allogeneic red blood cell transfusions and recommended supportive treatment with iron and erythropoietin analogues, avoiding further transfusion whenever possible.…”

Section: Association With Blood Transfusionmentioning

confidence: 99%

Immune hemolytic anemia—selected topics

Hoffman¹

2009

Hematology

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Autoimmune hemolytic anemia (AIHA) is most often idiopathic. However, in recent years, AIHA has been noted with increased incidence in patients receiving purine nucleoside analogues for hematologic malignancies; it has also been described as a complication of blood transfusion in patients who have also had alloimmunization. As the technology of hematopoietic stem cell transplantation has become more widespread, immune hemolysis in the recipients of ABO-mismatched products has become better recognized. The syndrome is caused by passenger lymphocytes transferred from the donor and, although transient, can be quite severe. A similar syndrome has been observed in recipients of solid organ transplants when there is ABO-incompatibility between donor and recipient. Venous thromboembolism is a little-recognized, though likely common, complication of AIHA, and may in some instances be related to coexistent antiphospholipid antibodies. While AIHA is a well-documented complication of malignant lymphoproliferative disorders, lymphoproliferative disorders may also paradoxically appear as a consequence of AIHA. A number of newer options are available for treatment of AIHA in patients refractory to corticosteroids and splenectomy. Newer immunosuppressives such as mycophenolate mofetil may have a role in such cases. Considerable experience has been accumulating in the last few years with monoclonal antibody therapy, mainly rituximab, in difficult AIHA cases; it appears to be a safe and effective option.

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Section: Association With Blood Transfusionmentioning

confidence: 99%

Immune hemolytic anemia—selected topics

Hoffman¹

2009

Hematology

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“…However, alloimmunization to minor red blood cell (RBC) antigens is frequent in chronically transfused recipients. In such transfused patients, almost 50% will have developed alloantibodies by adulthood, with a significant portion having made alloantibodies to several red cell antigens [3] causing complications ranging in severity from life-threatening delayed hemolytic transfusion reactions and autoimmunization to practical difficulties in obtaining matched blood [4][5][6][7]. While several factors including host genetics can influence the recipient's immune system to react to RBC alloantigens, the inflammatory status of transfusion recipients appears to be critical in determining the immunogenicity of transfused RBCs [8].…”

Section: Introductionmentioning

confidence: 99%

Prevention of red cell alloimmunization by CD25 regulatory T cells in mouse models

Heck

Yazdanbakhsh

2007

American J Hematol

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Transfusion therapy is currently an effective therapeutic intervention in a number of diseases, including sickle cell disease. However, its use is complicated by a high incidence of red blood cell (RBC) alloimmunization in the transfusion recipients. The identification of T regulatory cells (Tregs) among the CD4 þ CD25 þ T cell subset as key regulators of peripheral tolerance in mice as well as humans has opened an exciting era in the prevention and treatment of autoimmune disease and for improving organ transplantation. However, their potential in inducing transfusion tolerance remains to be explored. We used red cells from mice transgenic for human glycophorin A blood group antigen as donor cells and transfused wild-type mice to induce alloantibodies, as an experimental system to study RBC alloimmunization. We found that depletion with anti-CD25 enhanced the alloantibody production, indicating that CD25 Tregs play an important role in regulation of alloantibody responses. More importantly, adoptive transfer of purified population of-cells from naïve mice prevented the induction of IgG and IgM alloantibody production in transfusion recipients, with a concomitant reduction in activated splenic B cells and macrophages. Similarly, adoptive transfer of purified populations of CD4 þ CD25 þ cells from naïve mice into naïve syngeneic recipients inhibited the anti-Ig response to rat RBCs in the recipients but transfer of control CD4 þ CD25 -cells did not. Altogether, our results demonstrate that Tregs participate in the control of transfusion-associated RBC alloantibody responses, opening up the possibility that Treg immunotherapy may be exploited for suppressing transfusion immunization events. Am. J. Hematol. 82:691-696, 2007.

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“…Repeated transfusions can increase the risk of alloimmune response, and AHA is a potential complication of allogeneic blood transfusion that develops concomitantly or shortly after the transfusion. In those cases, supportive treatment with iron and erythropoietin, avoiding blood transfusion whenever possible, is recommended 4,5 . Unfortunately, the preparation and selection processes of blood for patients with AHA is slow, intensive, complicated, and expensive, and it is very difficult to find compatible blood even when a specificity is found.…”

Section: Discussionmentioning

confidence: 99%