2024-03-29T02:34:01Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1149682021-06-14T11:25:10Zcom_10261_79com_10261_1col_10261_332
Calderón, Jossela
Maganto-García, Elena
Punzón, Carmen
Carrión, Javier
Terhorst, Cox
Fresno, Manuel
2015-05-11T09:12:05Z
2015-05-11T09:12:05Z
2015-05-11
1553-7374
http://hdl.handle.net/10261/114968
Trypanosoma cruzi, the protozoan parasite responsible for Chagas' disease, causes severe myocarditis often resulting in death. Here, we report that Slamf1-/- mice, which lack the hematopoietic cell surface receptor Slamf1, are completely protected from an acute lethal parasite challenge. Cardiac damage was reduced in Slamf1-/- mice compared to wild type mice, infected with the same doses of parasites, as a result of a decrease of the number of parasites in the heart even the parasitemia was only marginally less. Both in vivo and in vitro experiments reveal that Slamf1-defIcient myeloid cells are impaired in their ability to replicate the parasite and show altered production of cytokines. Importantly, IFN-γ production in the heart of Slamf1 deficient mice was much lower than in the heart of wt mice even though the number of infiltrating dendritic cells, macrophages, CD4 and CD8 T lymphocytes were comparable. Administration of an anti-Slamf1 monoclonal antibody also reduced the number of parasites and IFN-γ in the heart. These observations not only explain the reduced susceptibility to in vivo infection by the parasite, but they also suggest human Slamf1 as a potential target for therapeutic target against T. cruzi infection.
eng
openAccess
The Receptor Slamf1 on the Surface of Myeloid Lineage Cells Controls Susceptibility to Infection by Trypanosoma cruzi
artículo