Increased interferon gamma production by peripheral blood mononuclear cells in response to stimulation of overexpressed disease-specific 9-O-acetylated sialoglycoconjugates in children suffering from acute lymphoblastic leukaemia

Increased interferon gamma production by peripheral blood mononuclear cells in response to stimulation of overexpressed disease-specific 9-O-acetylated sialoglycoconjugates in children suffering from acute lymphoblastic leukaemia
复制标题

DOI:
10.1111/j.1365-2141.2004.05256.x
复制
发表时间:
2005-01-01
影响因子:
6.5
通讯作者:
Mandal, C
Mandal, C
中科院分区:
医学2区
文献类型:
--
作者:
Ghosh, S;Bandyopadhyay, S;Mandal, C

文献摘要

被引文献

相似文献

已使用对9-O-AcSA α 2 - 6 GalNAc具有特异性的凝集素Achatinin-H证明了患有急性淋巴细胞白血病(ALL,PBMCALL)的儿童的外周血单核细胞(PBMC)上的9-O-乙酰化唾液酸糖缀合物(9-O-AcSG)的疾病特异性过表达。本研究探讨了9-O-AcSGs诱导的PBMCALL的贡献作用。通过9-O-AcSGs用Achatin-H刺激PBMCALL导致淋巴增殖反应,与未刺激的细胞相比,干扰素-γ(IFN-γ)的产生显著增加,如通过酶联免疫吸附测定和mRNA表达所证明的。在相同的条件下,PBMCALL消融的O-乙酰化没有响应这样的刺激。总之,可以得出结论,过度表达的9-O-AcSG的刺激调节增殖的信号传导,导致IFN-γ的释放。这些分子的受控表达可能被用作治疗的潜在靶点,对ALL儿童有希望产生有益效果。
Disease-specific over-expression of 9-O-acetylated sialoglycoconjugates (9-O-AcSGs) on peripheral blood mononuclear cells (PBMC) of children with acute lymphoblastic leukaemia (ALL, PBMCALL) has been demonstrated using a lectin, Achatinin-H, with specificity towards 9-O-AcSAalpha2-6GalNAc. This study investigated the contributory role of 9-O-AcSGs induced on PBMCALL. Stimulation of PBMCALL with Achatinin-H through 9-O-AcSGs led to a lymphoproliferative response with a significantly increased interferon-gamma (IFN-gamma) production when compared with unstimulated cells as demonstrated by enzyme-linked immunosorbent assay and mRNA expression. Under identical conditions, PBMCALL ablated of O-acetylations did not respond to such stimulation. In summary, it may be concluded that stimulation of over-expressed 9-O-AcSGs regulate signalling for proliferation, leading to the release of IFN-gamma. Controlled expression of these molecules may be exploited as potential targets for therapy, promising beneficial effects to children with ALL.