Host Cell Signalling and Leishmania Mechanisms of Evasion
Leishmania parasites are able to secure their survival and propagation within their host by altering signalling pathways involved in the ability of macrophages to kill pathogens or to engage adaptive immune system. An important step in this immune evasion process is the activation of host protein ty...
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ftdoajarticles:oai:doaj.org/article:507e199eec694f429dbb0e08b60f5d36 2023-05-15T15:05:59+02:00 Host Cell Signalling and Leishmania Mechanisms of Evasion Marina Tiemi Shio Kasra Hassani Amandine Isnard Benjamin Ralph Irazu Contreras Maria Adelaida Gomez Issa Abu-Dayyeh Martin Olivier 2012-01-01T00:00:00Z https://doi.org/10.1155/2012/819512 https://doaj.org/article/507e199eec694f429dbb0e08b60f5d36 EN eng Hindawi Limited http://dx.doi.org/10.1155/2012/819512 https://doaj.org/toc/1687-9686 https://doaj.org/toc/1687-9694 1687-9686 1687-9694 doi:10.1155/2012/819512 https://doaj.org/article/507e199eec694f429dbb0e08b60f5d36 Journal of Tropical Medicine, Vol 2012 (2012) Arctic medicine. Tropical medicine RC955-962 article 2012 ftdoajarticles https://doi.org/10.1155/2012/819512 2022-12-31T05:37:01Z Leishmania parasites are able to secure their survival and propagation within their host by altering signalling pathways involved in the ability of macrophages to kill pathogens or to engage adaptive immune system. An important step in this immune evasion process is the activation of host protein tyrosine phosphatase SHP-1 by Leishmania. SHP-1 has been shown to directly inactivate JAK2 and Erk1/2 and to play a role in the negative regulation of several transcription factors involved in macrophage activation. These signalling alterations contribute to the inactivation of critical macrophage functions (e.g., Nitric oxide, IL-12, and TNF-α). Additionally, to interfere with IFN-γ receptor signalling, Leishmania also alters several LPS-mediated responses. Recent findings from our laboratory revealed a pivotal role for SHP-1 in the inhibition of TLR-induced macrophage activation through binding to and inactivating IL-1-receptor-associated kinase 1 (IRAK-1). Furthermore, we identified the binding site as an evolutionarily conserved ITIM-like motif, which we named kinase tyrosine-based inhibitory motif (KTIM). Collectively, a better understanding of the evasion mechanisms utilized by Leishmania parasite could help to develop more efficient antileishmanial therapies in the near future. Article in Journal/Newspaper Arctic Directory of Open Access Journals: DOAJ Articles Arctic Journal of Tropical Medicine 2012 1 14 |
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Open Polar |
collection |
Directory of Open Access Journals: DOAJ Articles |
op_collection_id |
ftdoajarticles |
language |
English |
topic |
Arctic medicine. Tropical medicine RC955-962 |
spellingShingle |
Arctic medicine. Tropical medicine RC955-962 Marina Tiemi Shio Kasra Hassani Amandine Isnard Benjamin Ralph Irazu Contreras Maria Adelaida Gomez Issa Abu-Dayyeh Martin Olivier Host Cell Signalling and Leishmania Mechanisms of Evasion |
topic_facet |
Arctic medicine. Tropical medicine RC955-962 |
description |
Leishmania parasites are able to secure their survival and propagation within their host by altering signalling pathways involved in the ability of macrophages to kill pathogens or to engage adaptive immune system. An important step in this immune evasion process is the activation of host protein tyrosine phosphatase SHP-1 by Leishmania. SHP-1 has been shown to directly inactivate JAK2 and Erk1/2 and to play a role in the negative regulation of several transcription factors involved in macrophage activation. These signalling alterations contribute to the inactivation of critical macrophage functions (e.g., Nitric oxide, IL-12, and TNF-α). Additionally, to interfere with IFN-γ receptor signalling, Leishmania also alters several LPS-mediated responses. Recent findings from our laboratory revealed a pivotal role for SHP-1 in the inhibition of TLR-induced macrophage activation through binding to and inactivating IL-1-receptor-associated kinase 1 (IRAK-1). Furthermore, we identified the binding site as an evolutionarily conserved ITIM-like motif, which we named kinase tyrosine-based inhibitory motif (KTIM). Collectively, a better understanding of the evasion mechanisms utilized by Leishmania parasite could help to develop more efficient antileishmanial therapies in the near future. |
format |
Article in Journal/Newspaper |
author |
Marina Tiemi Shio Kasra Hassani Amandine Isnard Benjamin Ralph Irazu Contreras Maria Adelaida Gomez Issa Abu-Dayyeh Martin Olivier |
author_facet |
Marina Tiemi Shio Kasra Hassani Amandine Isnard Benjamin Ralph Irazu Contreras Maria Adelaida Gomez Issa Abu-Dayyeh Martin Olivier |
author_sort |
Marina Tiemi Shio |
title |
Host Cell Signalling and Leishmania Mechanisms of Evasion |
title_short |
Host Cell Signalling and Leishmania Mechanisms of Evasion |
title_full |
Host Cell Signalling and Leishmania Mechanisms of Evasion |
title_fullStr |
Host Cell Signalling and Leishmania Mechanisms of Evasion |
title_full_unstemmed |
Host Cell Signalling and Leishmania Mechanisms of Evasion |
title_sort |
host cell signalling and leishmania mechanisms of evasion |
publisher |
Hindawi Limited |
publishDate |
2012 |
url |
https://doi.org/10.1155/2012/819512 https://doaj.org/article/507e199eec694f429dbb0e08b60f5d36 |
geographic |
Arctic |
geographic_facet |
Arctic |
genre |
Arctic |
genre_facet |
Arctic |
op_source |
Journal of Tropical Medicine, Vol 2012 (2012) |
op_relation |
http://dx.doi.org/10.1155/2012/819512 https://doaj.org/toc/1687-9686 https://doaj.org/toc/1687-9694 1687-9686 1687-9694 doi:10.1155/2012/819512 https://doaj.org/article/507e199eec694f429dbb0e08b60f5d36 |
op_doi |
https://doi.org/10.1155/2012/819512 |
container_title |
Journal of Tropical Medicine |
container_volume |
2012 |
container_start_page |
1 |
op_container_end_page |
14 |
_version_ |
1766337656491343872 |