alpha 4 Integrins and sialyl Lewis x modulation in chronic Chagas disease: further evidence of persistent immune activation

dc.creatorLaucella, Susana A.
dc.creatorRiarte, Adelina
dc.creatorPrado, Nilda Graciela
dc.creatorZapata, J
dc.creatorSegura, Elsa L.
dc.date2019-12-13T18:41:13Z
dc.date2019-12-13T18:41:13Z
dc.date2001-05
dc.date.accessioned2023-08-29T20:06:41Z
dc.date.available2023-08-29T20:06:41Z
dc.identifier0300-9475
dc.identifierhttp://sgc.anlis.gob.ar/handle/123456789/1508
dc.identifier10.1046/j.1365-3083.2001.00916.x
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8519255
dc.descriptionWe have previously shown that titers of soluble platelet selectin (s-P-selectin) and soluble vascular cell adhesion molecule-1 (s-VCAM-1) were increased in sera of patients with chronic Trypanosoma cruzi infection. In this study, we analyzed the expression of CD49d-integrins, that bind to VCAM-1, and sialyl Lewis x (SLe(x)), which binds selectins, in peripheral blood lymphocytes of 27 patients with Chagas' disease at different levels of disease severity. Patients with a mild form of Chagas' disease showed a lower number of CD49d(+) cells, in comparison with those with severe chronic cardiopathy. Decreased levels of CD49d(+) cells were detected in CD3(-) cell populations. Conversely, SLe(x) expression was found to be decreased in patients with severe Chagas' disease. Levels of soluble platelet endothelial cell adhesion molecule-1 (s-PECAM-1) were significantly increased in the plasma of patients with severe Chagas' disease while unaltered levels of MCP-1 were recorded. These data show that VCAM-1 and P-Selectin ligands are differentially expressed during the chronic phase of the Trypanosoma cruzi infection. These findings also reinforce a role of the P-selectin/SLe(x) adhesion pathway rather than very late antigen-4 (VLA-4)/VCAM-1, in the pathogenesis of Chagas' disease.
dc.languageen
dc.relationScandinavian journal of immunology
dc.rightsopen
dc.titlealpha 4 Integrins and sialyl Lewis x modulation in chronic Chagas disease: further evidence of persistent immune activation
dc.typeArtículo


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