B-cell-directed therapy for chronic graft-versus-host disease.

fetal alloimmune thrombocytopenia-a less invasive option? J Obstet study of the antenatal management of feto-maternal alloimmune thrombocytopenia. Antenatal noninvasive treatment of patients at risk for alloimmune thrombocytopenia without a history of intracranial hemorrhage. Am Hung C, et al. Antepartum treatment without early cordocentesis for standard-risk alloimmune thrombocytopenia: a randomized controlled trial.fied management to prevent recurrence in the subsequent affected fetus.maternal alloim-mune thrombocytopenia: antenatal therapy with IvIgG and steroids-more questions than answers. European Working Group on FMAIT. Tutschek B. Fetal alloimmune thrombocytopenia and maternal intravenous immunoglobin infusions. A less invasive treatment strategy to prevent intracranial hemorrhage in fetal and neonatal alloimmune thrombocytopenia. Menticoglou SM. Fetomaternal hemorrhage following funipuncture: increase in severity of maternal red-cell alloimmunization. Antenatal management of severe feto-maternal alloimmune throm-bocytopenia: HLA incompatibility may affect responses to fetal platelet transfusions. A lthough acute morbidity and mortality associated with allogeneic hematopoietic stem cell transplanta-tion have steadily decreased over the past 20 years, chronic graft-versus-host disease (GVHD) remains a common complication and few new treatment approaches have been identified during this period. Unfortunately, therefore, chronic GVHD remains a frequent long-term toxicity that often affects patients who might otherwise be cured of their primary disease. Our current knowledge of the immune pathophysiology of chronic GVHD is limited in part because few animal models have been developed that mimic the varied clinical manifestations of this disease in humans. 1 The effective prevention of chronic GVHD by the depletion of T cells from the stem cell graft demonstrates that donor T cells play a critical role in this disease. When patients and donors are HLA-matched, minor histocom-patability antigens expressed in normal tissues of the recipient have been shown to elicit both CD4 + and CD8 + T-cell responses which result in either direct cell killing or cytokine-induced tissue injury. Thus, current therapies for chronic GVHD are targeted primarily and non-specifically against donor T-cell activity. Although donor T cells play a central role in the development of chronic GVHD, there is emerging evidence that donor B cells also contribute to the clinical manifestations of this disease. 2 In a mouse model of major histocompata-bility complex-mismatched transplantation, donor B cells were found to be necessary for the development of chronic GVHD. 3 In humans, at least some of these B cells produce known autoantibodies. 4 Our laboratory has previously shown that Y chromosome-encoded minor histocompata-bility antigens elicit specific antibody responses following sex-mismatched hematopoietic stem cell transplantation, and …