Long-term survival after allogeneic hematopoietic stem cell transplantation requires intact immunosurveillance, which is hampered by lymphoid organ damage associated with conditioning therapy, @entity2132 , and immunosuppression. Our study aimed to identify the mechanisms contributing to sustained low memory B  cell numbers after transplantation. Peripheral B and T  cell subset recovery and functional marker expression were investigated in 35 acute @entity1778 @entity1 up to 1  year after transplantation. Apoptosis of B  cells after @entity2936 / @entity6801 , @entity2936 /BCR, and @entity2936 /BCR/ @entity6801 -dependent stimulation and drug efflux capacity were analyzed. One half of the @entity1 suffered from infections after day 180. All @entity1 had strongly diminished @entity2731 (+) memory B  cells despite already normalized total B  cell numbers and fully recovered @entity2731 (-)IgD(-) memory B  cells, putatively of extra-follicular origin. Circulating memory follicular helper T  cells were reduced in the majority of @entity1 as well. Na  ve B  cells exhibited a decreased expression of @entity22750 , which mediates follicular B  cell entry. Additionally, a lower HLA-DR expression was found on na  ve B  cells, impairing antigen presentation. Upon @entity2936 / @entity6801 -dependent activation, B  cells underwent significantly increased apoptosis paralleled by an aberrant up-regulation of @entity12 on activated T  cells and Fas on resting B  cells. Significantly increased B  cell apoptosis was also observed after @entity2936 /BCR and @entity2936 /BCR/ @entity6801 -dependent activation. Drug efflux capacity of na  ve B  cells was diminished in @entity205 -treated @entity1 , additionally contributing to an apoptosis-prone phenotype. We conclude that B  cell survival and migration and T  cell communication defects are contributing candidates for an impaired germinal center formation of memory B  cells after allogeneic hematopoietic stem cell transplantation. Follow-up studies should evaluate effectiveness of revaccinations on the cellular level and should address the long-term sequelae of B  cell defects after transplantation.

Apoptosis Susceptibility Prolongs the Lack of Memory B Cells in Acute XXXX @entity1 After Allogeneic Hematopoietic Stem Cell Transplantation.

@entity1 :: ('9606', 'Species') :: ['patients'] @entity2936 :: ('958', 'Gene') :: ['CD40'] @entity6801 :: ('54106', 'Gene') :: ['TLR-9'] @entity22750 :: ('643', 'Gene') :: ['CXCR5'] @entity205 :: ('MESH:D016572', 'Chemical') :: ['cyclosporin A'] @entity1778 :: ('MESH:D007938', 'Disease') :: ['leukemic'] @entity2132 :: ('MESH:D006086', 'Disease') :: ['graft-versus-host disease'] @entity12 :: ('356', 'Gene') :: ['Fas-L'] @entity2731 :: ('939', 'Gene') :: ['CD27']
@entity1778 :: (MESH:D007938,Disease) :: ['Leukemic']
