Sialylated ligands on pathogenic Trypanosoma cruzi interact with Siglec-E (sialic acid-binding Ig-like lectin-E).
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Sialylated ligands on pathogenic Trypanosoma cruzi interact with Siglec-E (sialic acid-binding Ig-like lectin-E). / Erdmann, Hanna; Steeg, Christiane; Koch Nolte, Friedrich; Fleischer, Bernhard; Jacobs, Thomas.
In: CELL MICROBIOL, Vol. 11, No. 11, 11, 2009, p. 1600-1611.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - Sialylated ligands on pathogenic Trypanosoma cruzi interact with Siglec-E (sialic acid-binding Ig-like lectin-E).
AU - Erdmann, Hanna
AU - Steeg, Christiane
AU - Koch Nolte, Friedrich
AU - Fleischer, Bernhard
AU - Jacobs, Thomas
PY - 2009
Y1 - 2009
N2 - Trypanosoma cruzi causes a suppression of the immune system leading to persistence in host cells. The trans-sialidase (TS) expressed by T. cruzi is a major virulence factor and transfers sialic acid from host glycoconjugates to mucin-like molecules on the parasite. Here we demonstrate that these sialylated structures play a role in the immunosuppression. We used two T. cruzi strains, whose TS-activity correlated with their pathogenicity. The Tulahuen strain, characterized by a high TS-activity efficiently infected mice, whereas the Tehuantepec strain showing a reduced TS-activity could not establish a patent parasitemia. In vitro analysis revealed that these two strains invaded phagocytic and non-phagocytic host cells at a comparable rate, but they exhibited different potentials to modulate dendritic cell (DC) function. In contrast to Tehuantepec, the Tulahuen strain suppressed the production of the proinflammatory cytokine IL-12 and subsequent T cell activation. This inhibitory effect was absent upon desialylation of the parasite. Therefore, we analyzed whether sialylated structures of T. cruzi interact with the inhibitory sialic acid-binding protein Siglec-E on DC. Indeed, Siglec-E interacted with the pathogenic Tulahuen strain, but showed a diminished binding to the Tehuantepec strain. Ligation of Siglec-E on DC using antibodies confirmed this inhibitory effect on DC function.
AB - Trypanosoma cruzi causes a suppression of the immune system leading to persistence in host cells. The trans-sialidase (TS) expressed by T. cruzi is a major virulence factor and transfers sialic acid from host glycoconjugates to mucin-like molecules on the parasite. Here we demonstrate that these sialylated structures play a role in the immunosuppression. We used two T. cruzi strains, whose TS-activity correlated with their pathogenicity. The Tulahuen strain, characterized by a high TS-activity efficiently infected mice, whereas the Tehuantepec strain showing a reduced TS-activity could not establish a patent parasitemia. In vitro analysis revealed that these two strains invaded phagocytic and non-phagocytic host cells at a comparable rate, but they exhibited different potentials to modulate dendritic cell (DC) function. In contrast to Tehuantepec, the Tulahuen strain suppressed the production of the proinflammatory cytokine IL-12 and subsequent T cell activation. This inhibitory effect was absent upon desialylation of the parasite. Therefore, we analyzed whether sialylated structures of T. cruzi interact with the inhibitory sialic acid-binding protein Siglec-E on DC. Indeed, Siglec-E interacted with the pathogenic Tulahuen strain, but showed a diminished binding to the Tehuantepec strain. Ligation of Siglec-E on DC using antibodies confirmed this inhibitory effect on DC function.
M3 - SCORING: Zeitschriftenaufsatz
VL - 11
SP - 1600
EP - 1611
JO - CELL MICROBIOL
JF - CELL MICROBIOL
SN - 1462-5814
IS - 11
M1 - 11
ER -