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Reduced tumour necrosis factor receptor superfamily 13 C inversely correlated with tumour necrosis factor superfamily 13 B in patients with immune thrombocytopenia
Author(s) -
Zhu Xiaojuan,
Shi Yan,
Zhang Feng,
Yao Qingmin,
Liu Yanxia,
Shan Ningning,
Wang Dan,
Peng Jun,
Xu Jian,
Hou Ming
Publication year - 2014
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/bjh.12958
Subject(s) - flow cytometry , tumor necrosis factor alpha , immune system , necrosis , receptor , medicine , pathogenesis , cd19 , immunology , biology , endocrinology
Summary To investigate the expression of tumour necrosis factor superfamily 13 B ( TNFSF 13 B ) receptors in immune thrombocytopenia ( ITP ) and their correlation with disease activity, we investigated the protein and m RNA levels of TNFSF 13 B , tumour necrosis factor receptor superfamily 13 C ( TNFRSF 13 C ), TNFRSF 13 B and TNFRSF 17 by flow cytometry, enzyme‐linked immunosorbent assay and real time quantitative polymerase chain reaction. All CD 19 + B lymphocytes expressed TNFRSF13C by flow cytometry, but the mean fluorescence intensity ( MFI ) was decreased in patients with active disease compared to patients in remission and healthy controls, while no significant difference of TNFRSF 13 C m RNA was found between ITP patients and controls. The m RNA and plasma TNFSF 13 B were elevated in active ITP patients, and TNFRSF 13 C MFI level was inversely correlated with plasma TNFSF 13 B in active patients. In vitro assays showed that TNFRSF 13 C MFI was decreased after long exposure to TNFSF 13 B . No significant difference for TNFRSF 13 B or TNFRSF 17 was found between ITP patients and controls. In conclusion, TNFRSF 13 C expression is reduced on CD 19 + cells in active ITP patients. This down‐regulation occurs through a post‐transcriptional mechanism and could be a consequence of chronic increase of TNFSF 13 B .