Innate and Adaptive Immunity to Transfused Allogeneic RBCs in Mice Requires MyD88.

Innate and Adaptive Immunity to Transfused Allogeneic RBCs in Mice Requires MyD88.
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DOI:
10.4049/jimmunol.2100784
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发表时间:
2022-02-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Eisenbarth SC
Eisenbarth SC
中科院分区:
其他
文献类型:
--
作者:
Soldatenko A;Hoyt LR;Xu L;Calabro S;Lewis SM;Gallman AE;Hudson KE;Stowell SR;Luckey CJ;Zimring JC;Liu D;Santhanakrishnan M;Hendrickson JE;Eisenbarth SC

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Red blood cell (RBC) transfusion therapy is essential for the treatment of anemia. A serious complication of transfusion is the development of non-ABO alloantibodies to polymorphic RBC antigens, yet mechanisms of alloantibody formation remain unclear. Storage of mouse RBCs prior to transfusion increases RBC immunogenicity through an unknown mechanism. We previously reported that sterile, stored mouse RBCs activate splenic dendritic cells (DCs), which are required for alloimmunization. Here we transfused mice with allogeneic RBCs to test whether stored RBCs activate pattern recognition receptors (PRRs) on recipient DCs to induce adaptive immunity. Toll-like receptors are a class of PRRs that regulate DC activation, which signal through two adaptor molecules, MyD88 and TRIF. We show that the inflammatory cytokine response, DC activation and migration, and the subsequent alloantibody response to transfused RBCs require MyD88 but not TRIF, suggesting a restricted set of PRRs are responsible for sensing RBCs and triggering alloimmunization.
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