ArticleResearch and practice in thrombosis and haemostasis2026
A red blood cell-based antigen delivery system to facilitate T cell epitope presentation to promote peripheral tolerance to ADAMTS13 in immune-mediated thrombotic thrombocytopenic purpura.
Article in Research and practice in thrombosis and haemostasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Immunopeptidomics of blood coagulation factor IX: a core peptide derived from the protease domain is promiscuously presented on HLA-DR.Research and practice in thrombosis and haemostasis · 2026Article
- Solving another piece of the thrombotic thrombocytopenic purpura puzzle?Research and practice in thrombosis and haemostasis · 2026Article
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8 authors.
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Abstract
Background: Immune-mediated thrombotic thrombocytopenic purpura (iTTP) is a rare and potentially fatal autoimmune disease caused by a severe ADAMTS13 functional deficiency, mediated by autoantibodies targeting ADAMTS13. Despite high survival rates achieved with current treatments, between 20% and 50% of patients experience relapses. Ensuring longer-lasting recovery by restoring immune tolerance toward ADAMTS13 remains a significant unmet need. Objectives: To address this, we aimed to exploit the tolerogenic nature of the red blood cell (RBC) clearance pathway by using RBCs as antigen carriers. This approach allows for persistent exposure to ADAMTS13-derived peptides, promoting antigen-specific attenuation of autoreactive CD4 Methods: Specifically, we designed a fusion peptide comprising the trans-activator of transcription cell-penetrating peptide and an immunodominant ADAMTS13-derived T cell epitope (FINVAPHAR core amino acid sequence) to enable RBC surface loading. Results: We found that the fusion peptide binds to RBCs in a concentration-dependent manner. To assess whether our approach supports antigen presentation via human leukocyte antigen (HLA) class II molecules, macrophages were incubated with peptide-loaded RBCs, followed by analysis of HLA-DR-bound peptides via mass spectrometry. FINVAPHAR-containing peptides of varying lengths were mainly presented on macrophages from donors carrying the iTTP-associated HLA risk allele DRB1∗11, confirming functional antigen presentation and supporting the biological relevance of our model. Hemoglobin-derived peptides were also abundantly presented, supporting erythrophagocytosis as the entry route of our trans-activator of transcription-FINVAPHAR fusion peptide. Conclusion: Based on our results, we propose RBC-mediated delivery of ADAMTS13-derived peptides as a potential strategy for promoting tolerance in patients with iTTP.
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