ArticleFrontiers in immunology2016
Regulatory T Cells Are Dispensable for Tolerance to RBC Antigens.
Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The Immunology of Transfusion Medicine: Past, Present, and Future.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Development and consequences of red blood cell autoantibodies: warm autoimmune hemolytic anemia.Current opinion in immunology · 2025Review
- Article
- Regulatory T-cell dysfunctions are associated with increase in tumor necrosis factor α in autoimmune hemolytic anemia and participate in Th17 polarization.Haematologica · 2024Article
- Review
- A New Murine Model of Primary Autoimmune Hemolytic Anemia (AIHA).Frontiers in immunology · 2021Article
- Autoimmune hemolytic anemia: current knowledge and perspectives.Immunity & ageing : I & A · 2020Review
- Advances in the role of helper T cells in autoimmune diseases.Chinese medical journal · 2020Review
- The Role of mTOR Inhibitors in Hematologic Disease: From Bench to Bedside.Frontiers in oncology · 2020Review
- The Role of T Follicular Helper Cells and T Follicular Regulatory Cells in the Pathogenesis of Autoimmune Hemolytic Anemia.Scientific reports · 2019Article
- Murine models of autoimmune hemolytic anemia.Current opinion in hematology · 2018Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune hemolytic anemia (AIHA) occurs when pathogenic autoantibodies against red blood cell (RBC) antigens are generated. While the basic disease pathology of AIHA is well studied, the underlying mechanism(s) behind the failure in tolerance to RBC autoantigens are poorly understood. Thus, to investigate the tolerance mechanisms required for the establishment and maintenance of tolerance to RBC antigens, we developed a novel murine model. With this model, we evaluated the role of regulatory T cells (Tregs) in tolerance to RBC-specific antigens. Herein, we show that neither sustained depletion of Tregs nor immunization with RBC-specific proteins in conjunction with Treg depletion led to RBC-specific autoantibody generation. Thus, these studies demonstrate that Tregs are not required to prevent autoantibodies to RBCs and suggest that other tolerance mechanisms are likely involved.
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