AI Article Synopsis
- RBC transfusion therapy is crucial for treating anemia, but it can lead to complications like the development of non-ABO alloantibodies due to unclear mechanisms.
- Research indicates that storing mouse RBCs increases their ability to trigger immune responses, particularly through activation of splenic dendritic cells (DCs).
- Findings show that the activation of DCs and the resulting antibody response require the MyD88 adapter molecule in TLR signaling, rather than TRIF, highlighting specific pathways for detecting transfused RBCs and initiating immune responses.
Article Abstract
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 Ags; yet, mechanisms of alloantibody formation remain unclear. Storage of mouse RBCs before 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. TLRs are a class of PRRs that regulate DC activation, which signal through two adapter 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 that a restricted set of PRRs are responsible for sensing RBCs and triggering alloimmunization.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10107373 | PMC |
| http://dx.doi.org/10.4049/jimmunol.2100784 | DOI Listing |
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