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- 저자 : Celada, Antonio (검색결과 1 건)
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Castro de Moura, Manuel,Miro, Francesc,Han, Jung Min,Kim, Sunghoon,Celada, Antonio,Ribas de Pouplana, Lluí,s Public Library of Science 2011 PLoS neglected tropical diseases Vol.5 No.11
<▼1><P>Immunological pressure encountered by protozoan parasites drives the selection of strategies to modulate or avoid the immune responses of their hosts. Here we show that the parasite <I>Entamoeba histolytica</I> has evolved a chemokine that mimics the sequence, structure, and function of the human cytokine HsEMAPII (<I>Homo sapiens</I> endothelial monocyte activating polypeptide II). This <I>Entamoeba</I> EMAPII-like polypeptide (EELP) is translated as a domain attached to two different aminoacyl-tRNA synthetases (aaRS) that are overexpressed when parasites are exposed to inflammatory signals. EELP is dispensable for the tRNA aminoacylation activity of the enzymes that harbor it, and it is cleaved from them by <I>Entamoeba</I> proteases to generate a standalone cytokine. Isolated EELP acts as a chemoattractant for human cells, but its cell specificity is different from that of HsEMAPII. We show that cell specificity differences between HsEMAPII and EELP can be swapped by site directed mutagenesis of only two residues in the cytokines' signal sequence. Thus, <I>Entamoeba</I> has evolved a functional mimic of an aaRS-associated human cytokine with modified cell specificity.</P></▼1><▼2><P><B>Author Summary</B></P><P>Amebiasis caused by the parasite <I>Entamoeba histolytica</I> is one of the leading causes of dysentery worldwide, with an estimated annual mortality of 100.000. In 10% of patients, the intestinal infection can spread to internal organs causing hepatic, lung, and brain abscesses. Little is known about the strategies used by the parasite to evade or minimize the inflammatory and immune responses of its host. In this manuscript we report the discovery that <I>Entamoeba</I> has evolved a polypeptide that functionally mimics the activity of a human cytokine (EMAPII) involved in the regulation of inflammation. This polypeptide termed EELP (<I>Entamoeba</I> EMAPII-Like Polypeptide) is capable of attracting human cells, just like its human counterpart but, unlike EMAPII, EELP does not act on inflammatory cells. We have characterized the dynamics of gene expression that regulate EELP synthesis, and we demonstrate that the protein is produced when <I>Entamoeba</I> encounter inflammation signals produced by their human host. Our working hypothesis is that EELP is used by the parasite to shield itself from human inflammation. In general, the discovery of EELP opens a new avenue of research into the mechanisms used by <I>Entamoeba</I> to survive their host's environment.</P></▼2>
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