PMID- 20628793
OWN - NLM
STAT- MEDLINE
DCOM- 20110601
LR  - 20211020
IS  - 1573-2592 (Electronic)
IS  - 0271-9142 (Linking)
VI  - 30
IP  - 6
DP  - 2010 Nov
TI  - Direct B-cell stimulation by peripheral blood monocyte-derived dendritic cells in 
      idiopathic thrombocytopenic purpura patients.
PG  - 814-22
LID - 10.1007/s10875-010-9443-0 [doi]
AB  - OBJECTIVE: Dendritic cells (DCs) play a major role in regulating lymphocytes. The 
      emergence of antiplatelet autoantibodies remains the central pathogenetic 
      mechanism in idiopathic thrombocytopenic purpura (ITP); defective DC functions 
      have been implicated in ITP. The purpose of this study was to assess the 
      contribution of DCs to B-cell hyperactivity in ITP patients. METHODS: Ten ITP 
      patients were studied before treatment (group untreated) and after treatment 
      (group treated ) with improvement. We compared the effects of monocyte-derived DC 
      from ITP and healthy control (group control) on naive B cells in the presence of 
      lipopolysaccharide, or anti-CD40. We measured the proliferation, antibody 
      production, and expression of activation markers for B cells, as well as 
      DC-secreted B-cell activating factor (BAFF) production. We also measured the 
      serum BAFF level in ITP patients and control. The role of DC-produced BAFF was 
      evaluated with anti-BAFF. RESULTS: Lipopolysaccharide, or anti-CD40, stimulated 
      DCs from group untreated increased B-cell proliferation and antibody production 
      as compared with DCs from group treated and group control. Cell-to-cell contact 
      was not necessary for the augmented effect of the ITP DCs. Anti-CD40 treatment 
      induced a higher production of BAFF in group untreated DCs. Serum BAFF levels, 
      supernatant BAFF from anti-CD40-activated DCs, and BAFF mRNA expression of 
      anti-CD40-activated DCs in group untreated were significantly higher than that in 
      group treated and group control. In ITP patients, there was positive correlation 
      among serum BAFF, supernatant BAFF, and BAFF mRNA levels, and there was negative 
      correlation between serum BAFF, supernatant BAFF, BAFF mRNA levels, and blood 
      platelet count. Blocking BAFF abrogated the effects of ITP DCs on naive B 
      partially. CONCLUSION: Activated monocyte-derived DCs from ITP patients directly 
      increase B-cell effector functions; this effect depends on soluble factors 
      released by activated DCs and cell-to-cell contact. This might play an important 
      role in the antibody production in ITP. DC-secreted BAFF is involved and might 
      contribute to disease development.
FAU - Zhou, Zhenhai
AU  - Zhou Z
AD  - Department of Hematology, The First Affiliated Hospital, Sun Yat-sen University, 
      Guangzhou, 510080 Guangdong Province, People's Republic of China. 
      zhouship@yahoo.com.cn
FAU - Li, Xiaoyin
AU  - Li X
FAU - Li, Juan
AU  - Li J
FAU - Su, Chang
AU  - Su C
FAU - Zhuang, Lan
AU  - Zhuang L
FAU - Luo, Shaokai
AU  - Luo S
FAU - Zhang, Ling
AU  - Zhang L
LA  - eng
PT  - Journal Article
DEP - 20100714
PL  - Netherlands
TA  - J Clin Immunol
JT  - Journal of clinical immunology
JID - 8102137
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Autoantibodies)
RN  - 0 (B-Cell Activating Factor)
RN  - 0 (CD40 Antigens)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 0 (TNFSF13B protein, human)
SB  - IM
MH  - Antibodies, Monoclonal/immunology/metabolism
MH  - Autoantibodies/immunology/metabolism
MH  - B-Cell Activating Factor/*biosynthesis/blood/genetics
MH  - B-Lymphocytes/immunology/*metabolism/pathology
MH  - Blood Platelets/immunology
MH  - CD40 Antigens/immunology
MH  - Cell Differentiation/immunology
MH  - Dendritic Cells/immunology/*metabolism/pathology
MH  - Humans
MH  - Lipopolysaccharides/immunology/metabolism
MH  - Lymphocyte Activation
MH  - Lymphocyte Subsets/immunology/*metabolism/pathology
MH  - Monocytes/pathology
MH  - Purpura, Thrombocytopenic, Idiopathic/blood/*immunology
MH  - RNA, Messenger/analysis
EDAT- 2010/07/16 06:00
MHDA- 2011/06/02 06:00
CRDT- 2010/07/15 06:00
PHST- 2010/05/15 00:00 [received]
PHST- 2010/07/01 00:00 [accepted]
PHST- 2010/07/15 06:00 [entrez]
PHST- 2010/07/16 06:00 [pubmed]
PHST- 2011/06/02 06:00 [medline]
AID - 10.1007/s10875-010-9443-0 [doi]
PST - ppublish
SO  - J Clin Immunol. 2010 Nov;30(6):814-22. doi: 10.1007/s10875-010-9443-0. Epub 2010 
      Jul 14.