Reduced transforming growth factor-β1 production by mononuclear cells from patients with active chronic idiopathic thrombocytopenic purpura

被引:54
作者
Andersson, PO [1 ]
Olsson, A [1 ]
Wadenvik, H [1 ]
机构
[1] Univ Gothenburg, Sahlgrenska Hosp, Dept Internal Med, Haematol Sect, S-41345 Gothenburg, Sweden
关键词
TGF-beta; 1; chronic ITP; Th3; cytokine; PBMC; active disease;
D O I
10.1046/j.0007-1048.2002.03345.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Chronic idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder in which activated T-helper (Th) cells and different Th-cell cytokines might play an important role. We have recently reported that chronic ITP patients in remission had elevated plasma levels of the Th3 cytokine transforming growth factor-beta1 (TGF-beta1). possibly as a part of a bystander immune suppression. In the present study we found that, in ITP patients with active disease [platelet count (plc) < 50 x 10(9)/l], mitogen-stimulated peripheral blood mononuclear cells (PBMC) had a significantly reduced production of TGF-beta 1 (444 178 pg/ml; n = 6) compared with patients with plc 50-150 x 10(9)/l (1293 +/- 374 pg/ml: n 9: P < 0.05), patients with plc > 150 x 10(9)/l (1894 244 pg/ml; n = 12: P < 0.005) and healthy controls (1698 241 pg/ml; n = 10; P < 0.01). Nineteen per cent of up patients expressed a platelet-induced PBMC proliferation. Surprisingly. 22% of the ITP patients had a PBMC proliferation below the normal range, i.e. a suppressed proliferation in the presence of platelets; live of these six patients had active disease. In summary. this study demonstrated that chronic ITP patients with active disease had reduced PBMC production of the Th3 cytokine TGF-beta1. This result gives further support to the theory that chronic ITP in active phase is associated with it downregulatcd Th3-response.
引用
收藏
页码:862 / 867
页数:6
相关论文
共 38 条
[1]   A transforming growth factor-β1-mediated bystander immune suppression could be associated with remission of chronic idiopathic thrombocytopenic purpura [J].
Andersson, PO ;
Stockelberg, D ;
Jacobsson, S ;
Wadenvik, H .
ANNALS OF HEMATOLOGY, 2000, 79 (09) :507-513
[2]  
Blanchette V, 1998, SEMIN HEMATOL, V35, P36
[3]   Transforming growth factor beta (TGF-beta)-dependent inhibition of T helper cell 2 (Th2)-induced autoimmunity by self-major histocompatibility complex (MHC) class II-specific, regulatory CD4(+) T cell lines [J].
Bridoux, F ;
Badou, A ;
Saoudi, A ;
Bernard, I ;
Druet, E ;
Pasquier, R ;
Druet, P ;
Pelletier, L .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (10) :1769-1775
[4]   REGULATORY T-CELL CLONES INDUCED BY ORAL TOLERANCE - SUPPRESSION OF AUTOIMMUNE ENCEPHALOMYELITIS [J].
CHEN, YH ;
KUCHROO, VK ;
INOBE, J ;
HAFLER, DA ;
WEINER, HL .
SCIENCE, 1994, 265 (5176) :1237-1240
[5]  
CROSS D, 1990, J IMMUNOL, V144, P432
[6]   Effects of interferon-alpha therapy on immune parameters in immune thrombocytopenic purpura [J].
Crossley, AR ;
Dickinson, AM ;
Proctor, SJ ;
Calvert, JE .
AUTOIMMUNITY, 1996, 24 (02) :81-100
[7]   Rapamycin induces transforming growth factor-β production by lymphocytes [J].
Dodge, IL ;
Demirci, G ;
Strom, TB ;
Li, XC .
TRANSPLANTATION, 2000, 70 (07) :1104-1106
[8]   Long-term salvage treatment by cyclosporin in refractory autoimmune haematological disorders [J].
Emilia, G ;
Messora, C ;
Longo, G ;
Bertesi, M .
BRITISH JOURNAL OF HAEMATOLOGY, 1996, 93 (02) :341-344
[9]  
Erduran E, 1998, AM J HEMATOL, V57, P119, DOI 10.1002/(SICI)1096-8652(199802)57:2<119::AID-AJH5>3.0.CO
[10]  
2-Z