Molecular interaction of Siglecs (sialic acid-binding Ig-like lectins) with sialylated ligands on Trypanosoma cruzi.

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Molecular interaction of Siglecs (sialic acid-binding Ig-like lectins) with sialylated ligands on Trypanosoma cruzi. / Jacobs, Thomas; Erdmann, Hanna; Fleischer, Bernhard.

In: EUR J CELL BIOL, 2009.

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@article{8040ad3ff92445509a56888a7fc029ec,
title = "Molecular interaction of Siglecs (sialic acid-binding Ig-like lectins) with sialylated ligands on Trypanosoma cruzi.",
abstract = "The protozoan parasite Trypanosoma cruzi (T. cruzi) is transmitted by blood-sucking insect vectors. After transmission, parasites circulate in the blood as trypomastigotes and invade a variety of cells to multiply intracellularly as amastigotes. The acute phase triggers an immune response that restricts the dissemination and proliferation of parasites. However, parasites are able to persist in different tissues for decades causing the pathology of Chagas' disease. T. cruzi expresses a trans-sialidase (TS). This unique enzyme transfers sialic acid from host glycoconjugates to mucin-like molecules on the parasite and is supposed to be a major virulence factor. TS and sialylated structures were implicated in the persistence of parasites. We discuss here the recent findings on the function of sialylated structures on the surface of T. cruzi with a special emphasis on their property to interact with sialic acid-binding Ig-like lectins, which may allow the parasite to modulate the immune system of the host.",
author = "Thomas Jacobs and Hanna Erdmann and Bernhard Fleischer",
year = "2009",
language = "Deutsch",
journal = "EUR J CELL BIOL",
issn = "0171-9335",
publisher = "Urban und Fischer Verlag GmbH und Co. KG",

}

RIS

TY - JOUR

T1 - Molecular interaction of Siglecs (sialic acid-binding Ig-like lectins) with sialylated ligands on Trypanosoma cruzi.

AU - Jacobs, Thomas

AU - Erdmann, Hanna

AU - Fleischer, Bernhard

PY - 2009

Y1 - 2009

N2 - The protozoan parasite Trypanosoma cruzi (T. cruzi) is transmitted by blood-sucking insect vectors. After transmission, parasites circulate in the blood as trypomastigotes and invade a variety of cells to multiply intracellularly as amastigotes. The acute phase triggers an immune response that restricts the dissemination and proliferation of parasites. However, parasites are able to persist in different tissues for decades causing the pathology of Chagas' disease. T. cruzi expresses a trans-sialidase (TS). This unique enzyme transfers sialic acid from host glycoconjugates to mucin-like molecules on the parasite and is supposed to be a major virulence factor. TS and sialylated structures were implicated in the persistence of parasites. We discuss here the recent findings on the function of sialylated structures on the surface of T. cruzi with a special emphasis on their property to interact with sialic acid-binding Ig-like lectins, which may allow the parasite to modulate the immune system of the host.

AB - The protozoan parasite Trypanosoma cruzi (T. cruzi) is transmitted by blood-sucking insect vectors. After transmission, parasites circulate in the blood as trypomastigotes and invade a variety of cells to multiply intracellularly as amastigotes. The acute phase triggers an immune response that restricts the dissemination and proliferation of parasites. However, parasites are able to persist in different tissues for decades causing the pathology of Chagas' disease. T. cruzi expresses a trans-sialidase (TS). This unique enzyme transfers sialic acid from host glycoconjugates to mucin-like molecules on the parasite and is supposed to be a major virulence factor. TS and sialylated structures were implicated in the persistence of parasites. We discuss here the recent findings on the function of sialylated structures on the surface of T. cruzi with a special emphasis on their property to interact with sialic acid-binding Ig-like lectins, which may allow the parasite to modulate the immune system of the host.

M3 - SCORING: Zeitschriftenaufsatz

JO - EUR J CELL BIOL

JF - EUR J CELL BIOL

SN - 0171-9335

ER -