Premium
High‐level serum B‐cell activating factor and promoter polymorphisms in patients with idiopathic thrombocytopenic purpura
Author(s) -
Emmerich Florian,
Bal Gürkan,
Barakat Alaa,
Milz Julian,
Mühle Caroline,
MartinezGamboa Lorena,
Dörner Thomas,
Salama Abdulgabar
Publication year - 2007
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2006.06431.x
Subject(s) - b cell activating factor , autoantibody , thrombocytopenic purpura , immunology , medicine , platelet , autoimmune disease , tumor necrosis factor alpha , autoimmunity , b cell , immune system , antibody
Summary Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder in which platelets are opsonised by autoantibodies and destroyed by macrophages. Therefore, ITP represents a prototype of a B‐cell‐mediated autoimmune disorder. B‐cell activating factor (BAFF) is a member of the tumour necrosis factor family and an important regulator of B‐cell development. BAFF levels were determined in serum samples from 53 patients with ITP. Serum BAFF levels in patients with an active ITP were increased when compared with the healthy control group (median 1620 pg/ml vs. 977 pg/ml; P < 0·001). Moreover, immunosuppressive treatment was associated with strongly suppressed BAFF levels (median 629 pg/ml; P < 0·01). In addition, a polymorphic site was detected in the BAFF promoter region (−871) that appeared to occur more frequently in ITP patients than in healthy persons. This promoter variant was associated with very high BAFF levels in ITP patients. Our data suggest that BAFF is an important pathogenetic factor in the development of ITP.