期刊
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
卷 183, 期 2, 页码 271-279出版社
WILEY-BLACKWELL
DOI: 10.1111/cei.12709
关键词
cysticerci; dendritic cells; neurocysticercosis; regulatory T cells; Taenia solium
类别
资金
- CONACYT [CB-2008-01 100708, CB-2011-01 167278]
- DGAPA, Mexico [IN213911]
Neurocysticercosis is caused by the establishment of Taenia solium cysticerci in the central nervous system. It is considered that, during co-evolution, the parasite developed strategies to modulate the host's immune response. The action mechanisms of regulatory T cells in controlling the immune response in neurocysticercosis are studied in this work. Higher blood levels of regulatory T cells with CD4(+)CD45RO(+)forkhead box protein 3 (FoxP3)(high) and CD4(+)CD25(high)FoxP3(+)CD95(high) phenotype and of non-regulatory CD4(+)CD45RO(+)FoxP3(med) T cells were found in neurocysticercosis patients with respect to controls. Interestingly, regulatory T cells express higher levels of cytotoxic T lymphocyte antigen 4 (CTLA-4), lymphocyte-activation gene 3 (LAG-3), programmed death 1 (PD-1) and glucocorticoid-induced tumour necrosis factor receptor (GITR), suggesting a cell-to-cell contact mechanism with dendritic cells. Furthermore, higher IL-10 and regulatory T cell type 1 (Tr1) levels were found in neurocysticercosis patients' peripheral blood, suggesting that the action mechanism of regulatory T cells involves the release of immunomodulatory cytokines. No evidence was found of the regulatory T cell role in inhibiting the proliferative response. Suppressive regulatory T cells from neurocysticercosis patients correlated negatively with late activated lymphocytes (CD4(+)CD38(+)). Our results suggest that, during neurocysticercosis, regulatory T cells could control the immune response, probably by a cell-to-cell contact with dendritic cells and interleukin (IL)-10 release by Tr1, to create an immunomodulatory environment that may favour the development of T. solium cysticerci and their permanence in the central nervous system.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据