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Publication Detail
A8.14 Effect of rituximab on B-cell phenotypes and on B-cell activating factor receptor expression in patients with thrombotic thrombocytopenic purpura.
Thrombotic Thrombocytopenic Purpura (TTP) is due to deficiency or dysfunction of the metalloproteinase ADAMTS13, which cleaves von Willebrand factor. This results in increased platelet adhesion and thrombus formation in small blood vessels. Most cases are associated with autoantibodies (IgM/IgG/IgA) to ADAMTS13, which are somatically mutated (sub-classes being predominantly IgG4 subclass, followed by IgG1). Rituximab (RTX) is an effective treatment for patients with TTP and also for patients with Rheumatoid Arthritis (RA). In both conditions, remission can last for months or even years after RTX but in RA, relapse closer to B-cell return is more common. Factors controlling B-cell maturation, differentiation and autoantibody production probably impact remission. Survival and maturation of B-cells largely depends on interactions with the B-cell cytokine B-cell activating factor (BAFF). In order to explore the possible role of the BAFF/BAFF-receptor (BAFF-R or BR3) system in maintaining long remissions following RTX in TTP patients, we investigated B-cell phenotypes, serum BAFF levels and BAFF-R expression. The relationship between time after treatment, B-cell phenotype and BAFF-R expression with laboratory parameters in TTP patients was also explored.
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