| Literature DB >> 29055003 |
Rahma Elayeb1,2,3, Marie Tamagne1,2,3, Marion Pinheiro1,2,3, Julie Ripa1,2,3, Rachid Djoudi1, Philippe Bierling1,2,3,4, France Pirenne5,2,3,4, Benoît Vingert5,2,3.
Abstract
Alloimmunization against RBCs can cause life-threatening delayed hemolytic transfusion reactions. Anti-CD20 Ab has recently been used to prevent alloimmunization. However, its effects remain unclear, particularly in lymphoid organs. We investigated the impact of murine anti-CD20 Ab in the blood and spleen. We assessed protocols for preventing primary alloimmunization and for abolishing established alloimmunization. Prophylactic protocols prevented alloimmunization. However, anti-CD20 treatment could only limit the further amplification of established alloimmunization. Residual B cell subtype distribution was disrupted in the spleen, but adoptive transfer studies indicated that these cells were neither plasma nor memory cells. Anti-CD20 Ab had a major effect on alloreactive CD4+ T cells, increasing the expansion of this population and its CD40 expression, while lowering its CD134 expression, thereby confirming its role in alloimmunization. In conclusion, this study shows that anti-CD20 immunotherapy can prevent RBC Ab development. However, this immunotherapy is limited by the increase in alloreactive CD4+ T lymphocytes. Nevertheless, treatment with anti-CD20 Abs should be considered for patients requiring transfusion with a very high risk of alloimmunization and life-threatening complications.Entities:
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Year: 2017 PMID: 29055003 DOI: 10.4049/jimmunol.1700754
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422