The excretory-secretory products of Echinococcus granulosus protoscoleces stimulated IL-10 production in B cells via TLR-2 signaling.
The excretory-secretory products of Echinococcus granulosus protoscoleces stimulated IL-10 production in B cells via TLR-2 signaling.
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细粒棘球蚴原头节的排泄分泌产物通过 TLR-2 信号刺激 B 细胞产生 IL-10
DOI:
10.1186/s12865-018-0267-7
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发表时间:
2018-10-24
期刊:
影响因子:
3
通讯作者:
Zheng KY
中科院分区:
文献类型:
--
作者:
Pan W;Xu HW;Hao WT;Sun FF;Qin YF;Hao SS;Liu H;Cao JP;Shen YJ;Zheng KY
Background:Excretory-secretory products released by Echinococcus granulosus protoscoleces (EgPSC-ESPs) are well-known to regulate T cell responses. However, their direct influence on the differentiation of B cell subsets remains largely elusive. This study investigated the effects of EgPSC-ESPs on the differentiation of IL-10-producing B cells (B10), and explored the possible role of Toll-like receptor 2 (TLR-2) signaling in this process.Results:In comparison to phosphate buffered saline (PBS), B cells exposed to the excretory-secretory products (ESPs) generated higher percentages of B10 cells, with higher expression of IL-10 mRNA, and larger amount of IL-10 production, which were in a dose dependent way. The mRNA and protein expression of TLR-2 in the ESPs-stimulated B cells were significantly higher than those in PBS, which was consistent to the results in B cells isolated from EgPSC infected mice. Moreover, TLR-2-/-B cells in response to ESPs stimulation expressed lower levels of IL-10 mRNA and produced undetectable IL-10 in comparison to those in normal B cells. In addition, Phosphatase and tensin homolog deleted on chromosome ten/AKT/Phosphatidylinositol-3 kinase (PTEN/AKT/PI3K) pathway was activated in ESPs-treated B cells, which was also dependent on TLR-2 signaling. Pam3CSK4, the agonist of TLR-2, could mock the effects of ESPs on the expression of PTEN, AKT and PI3K.Conclusion:Overall, this study revealed that TLR-2 signaling was required for B10 induction mediated by EgPSC-ESPs, which might be an immunomodulatory target against the parasite infection.
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影响因子:
3.2
作者:
Pan W;Hao WT;Shen YJ;Li XY;Wang YJ;Sun FF;Yin JH;Zhang J;Tang RX;Cao JP;Zheng KY
通讯作者:
Zheng KY
影响因子:
16.6
作者:
Dambuza IM;He C;Choi JK;Yu CR;Wang R;Mattapallil MJ;Wingfield PT;Caspi RR;Egwuagu CE
通讯作者:
Egwuagu CE
影响因子:
15.9
作者:
Matsushita, Takashi;Yanaba, Koichi;Tedder, Thomas F.
通讯作者:
Tedder, Thomas F.
影响因子:
2.4
作者:
Carmena, D;Martínez, J;Guisantes, JA
通讯作者:
Guisantes, JA
影响因子:
4.4
作者:
Lampropoulou, Vicky;Hoehlig, Kai;Fillatreau, Simon
通讯作者:
Fillatreau, Simon