2026-06-14T05:06:24Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/74742025-02-27T13:55:30Zcom_20.500.12105_2052com_20.500.12105_2051col_20.500.12105_19609
Repisalud
author
Dominguez-Rodriguez, Mercedes
author
Toraño, Alfredo
2019-04-22T10:26:18Z
2019-04-22T10:26:18Z
1999-01-04
J Exp Med. 1999;189(1):25-35.
0022-1007
The Journal of experimental medicine
https://pmc.ncbi.nlm.nih.gov/articles/PMC1887685/
9874561
http://hdl.handle.net/20.500.12105/7474
To mimic the sandfly pool feeding process and characterize the cellular and biochemical events that occur during the early stages of promastigote-host interaction, we developed an ex vivo model of human blood infection with Leishmania promastigotes. Within 30 s of blood contact, Leishmania promastigotes bind natural anti-Leishmania antibodies, which then activate the classical complement pathway and opsonization by the third component of complement. The opsonized promastigotes undergo an immune adherence reaction and bind quantitatively to erythrocyte CR1 receptors; opsonized Leishmania amastigotes also bind to erythrocytes. Progression of infection implies promastigote transfer from erythrocytes to acceptor blood leukocytes. After 10 min of ex vivo infection, 25% of all leukocytes contain intracellular parasites, indicating that blood cells are the early targets for the invading promastigotes. We propose that adaptation to the immune adherence mechanism aids Leishmania survival, promoting rapid promastigote phagocytosis by leukocytes. This facilitates host colonization and may represent the parasite's earliest survival strategy. In light of this mechanism, it is unlikely that infection-blocking vaccines can be developed.
eng
Leishmania
Infection
Immune adherence
Natural antibodies
Complement
Immune adherence-mediated opsonophagocytosis: the mechanism of Leishmania infection
research article