Role of Toll-like receptor 2 in primary immune thrombocytopenia.
10.7534/j.issn.1009-2137.2014.04.027
- Author:
Hui-Yuan LI
1
;
Dong-Lei ZHANG
1
;
Xian ZHANG
1
;
Rong-Feng FU
1
;
Min XUAN
1
;
Ren-Chi YANG
2
,
3
Author Information
1. Institute of Hematology & Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China.
2. Institute of Hematology & Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China. E-mail:rcyang65@
3. com.
- Publication Type:Journal Article
- MeSH:
Adolescent;
Adult;
Aged;
Case-Control Studies;
Cells, Cultured;
Child;
Female;
Humans;
Interleukin-6;
immunology;
Male;
Middle Aged;
RNA, Messenger;
genetics;
Thrombocytopenia;
immunology;
metabolism;
pathology;
Toll-Like Receptor 2;
metabolism;
Tumor Necrosis Factor-alpha;
immunology;
Young Adult
- From:
Journal of Experimental Hematology
2014;22(4):1033-1037
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to explore the role of Toll-like receptor (TLR) 2 in primary immune thrombocytopenia (ITP) by detecting TLR2 expression in the peripheral blood lymphocytes of patients with ITP and evaluating the role of TLR2 activation on inflammatory cytokine secretion. A total of 39 ITP patients and 21 normal controls were enrolled in this study. The expression of TLR2 was detected by real-time PCR and flow cytometry, and the concentration of IL-6 and TNF-α in culture supernatant of PBMNC treated with pam3CSK4 for 48 hours were detected by ELISA. The results showed that the expression of TLR2 mRNA in active ITP patients (3.561 ± 0.741) was significantly higher than that in normal controls (1.750 ± 0.314) (P < 0.05), but there was no statistically significant difference between remission ITP patients (2.333 ± 0.448) and normal controls (P > 0.05) . Flow cytometry analysis found that the TLR2 was not expressed on T and B cells, but expressed on all monocytes both from ITP patients and normal controls. Further activation experiment showed that TLR2 activation in vitro could induce the expression of IL-6 (1644 ± 634.0 vs 4111 ± 525.2 pg/ml) and TNF-α (75.37 ± 22.31 vs 326.0 ± 109.9 pg/ml) in PBMNC from ITP patients (both P < 0.05), but just could promote IL-6 expression in normal controls (2119 ± 636.9 vs 4671 ± 315.9 pg/ml)(P < 0.05). It is concluded that the expression of TLR2 mRNA is up-regulated in PBMNC of ITP patients, and this increased TLR2 maybe participate in ITP through inducing secretion of inflammatory cytokines.
