人树突状细胞成熟受 通过Akt信号通路调控。 你提供的原文似乎不太完整,“by”后面缺少具体内容。
Human Dendritic Cell Maturation Is Modulated by through Akt Signaling Pathway.
作者信息
Rodríguez-González Jorge, Wilkins-Rodríguez Arturo A, Gutiérrez-Kobeh Laila
机构信息
Laboratorio de Estudios Epidemiológicos, Clínicos, Diseños Experimentales e Investigación, Facultad de Ciencias Químicas, Universidad Autónoma Benito Juárez, Oaxaca C.P. 68120, Mexico.
Unidad de Investigación UNAM-INC, División de Investigación, Facultad de Medicina, Universidad Nacional Autónoma de México-Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano No. 1, Col. Sección XVI, Tlalpan, Mexico City C.P. 14080, Mexico.
出版信息
Trop Med Infect Dis. 2024 May 17;9(5):118. doi: 10.3390/tropicalmed9050118.
Dendritic cells (DC) along with macrophages are the main host cells of the intracellular parasite . DC traverse a process of maturation, passing through an immature state with phagocytic ability to a mature one where they can modulate the immune response through the secretion of cytokines. Several studies have demonstrated that inhibits DC maturation. Nevertheless, when cells are subjected to a second stimulus such as LPS/IFN-γ, they manage to mature. In the maturation process of DC, several signaling pathways have been implicated, importantly MAPK. On the other hand, Akt is a signaling pathway deeply involved in cell survival. Some species have shown to activate MAPK and Akt in different cells. The aim of this work was to investigate the role of ERK and Akt in the maturation of monocyte-derived DC (moDC) infected with . moDC were infected with metacyclic promastigotes, and the phosphorylation of ERK and Akt, the expression of MHCII and CD86 and IL-12 transcript, and secretion were determined in the presence or absence of an Akt inhibitor. We showed that induces a sustained Akt and ERK phosphorylation, while the Akt inhibitor inhibits it. Moreover, the infection of moDC downregulates CD86 expression but not MHCII, and the Akt inhibitor reestablishes CD86 expression and 12p40 production. Thus, can modulate DC maturation though Akt signaling.
树突状细胞(DC)与巨噬细胞一起是细胞内寄生虫的主要宿主细胞。DC经历一个成熟过程,从具有吞噬能力的未成熟状态转变为能够通过分泌细胞因子来调节免疫反应的成熟状态。多项研究表明,[病原体名称未给出]抑制DC成熟。然而,当细胞受到诸如LPS/IFN-γ等第二种刺激时,它们能够成熟。在DC的成熟过程中,涉及多种信号通路,重要的是丝裂原活化蛋白激酶(MAPK)。另一方面,Akt是一条深度参与细胞存活的信号通路。一些[病原体名称未给出]物种已显示在不同细胞中激活MAPK和Akt。这项工作的目的是研究细胞外信号调节激酶(ERK)和Akt在感染[病原体名称未给出]的单核细胞衍生DC(moDC)成熟中的作用。用[病原体名称未给出]循环前鞭毛体感染moDC,并在存在或不存在Akt抑制剂的情况下测定ERK和Akt的磷酸化、主要组织相容性复合体II类分子(MHCII)和CD86的表达以及白细胞介素12(IL-12)转录本和分泌情况。我们发现,[病原体名称未给出]诱导Akt和ERK持续磷酸化,而Akt抑制剂可抑制这种磷酸化。此外,moDC感染下调CD86表达但不影响MHCII表达,Akt抑制剂可恢复CD86表达和IL-12p40产生。因此,[病原体名称未给出]可通过Akt信号传导调节DC成熟。
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