Mechanisms of immune evasion in leishmaniasis
- PMID: 23415155
- PMCID: PMC3697132
- DOI: 10.1016/B978-0-12-407679-2.00005-3
Mechanisms of immune evasion in leishmaniasis
Abstract
Diseases caused by Leishmania present a worldwide problem, and current therapeutic approaches are unable to achieve a sterile cure. Leishmania is able to persist in host cells by evading or exploiting host immune mechanisms. A thorough understanding of these mechanisms could lead to better strategies for effective management of Leishmania infections. Current research has focused on parasite modification of host cell signaling pathways, entry into phagocytic cells, and modulation of cytokine and chemokine profiles that alter immune cell activation and trafficking to sites of infection. Immuno-therapeutic approaches that target these mechanisms of immune evasion by Leishmania offer promising areas for preclinical and clinical research.
Copyright © 2013 Elsevier Inc. All rights reserved.
References
-
- Afonso L, Borges VM, Cruz H, Ribeiro-Gomes FL, DosReis GA, Dutra AN, et al. Interactions with apoptotic but not with necrotic neutrophils increase parasite burden in human macrophages infected with Leishmania amazonensis. Journal of Leukocyte Biology. 2008;84:389–396. - PubMed
-
- Alexander J, Satoskar AR, Russell DG. Leishmania species: models of intracellular parasitism. Journal of Cell Science. 1999;112(Pt 18):2993–3002. - PubMed
Publication types
MeSH terms
Substances
Grants and funding
- R34AI100789/AI/NIAID NIH HHS/United States
- R34 AI100789/AI/NIAID NIH HHS/United States
- R56 AI090803/AI/NIAID NIH HHS/United States
- R03CA164399/CA/NCI NIH HHS/United States
- R21 AI076309/AI/NIAID NIH HHS/United States
- RC4 AI092624/AI/NIAID NIH HHS/United States
- R03 AI090231/AI/NIAID NIH HHS/United States
- R03AI090231/AI/NIAID NIH HHS/United States
- R21AT004160/AT/NCCIH NIH HHS/United States
- T32 DE014320/DE/NIDCR NIH HHS/United States
- T32DE014320/DE/NIDCR NIH HHS/United States
- R21 AT004160/AT/NCCIH NIH HHS/United States
- R03 CA164399/CA/NCI NIH HHS/United States
- RC4AI092624/AI/NIAID NIH HHS/United States
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
