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Leishmanial apolipoprotein A-I expression: a possible strategy used by the parasite to evade the host’s immune response

Department of Immunology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

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Raúl Manzano-Román

Proteomics Unit, Cancer Research Centre (IBMCC/CSIC/USAL/IBSAL), Salamanca, 37007, Spain

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Esmaeel Ghani

Endocrinology and Metabolism Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran

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Reza Mansouri

Department of Immunology, Faculty of Medicine, Shahid Sadoughi University of Medical Sciences & Health Services, Yazd, Iran

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Gholamreza Hatam

Basic Sciences in Infectious Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

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Paul Nguewa

**Author for correspondence:

E-mail Address: panguewa@unav.es

Department of Microbiology & Parasitology, University of Navarra, ISTUN Instituto de Salud Tropical, IdiSNA (Navarra Institute for Health Research), c/ Irunlarrea 1, Pamplona, 31008, Spain

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Sajad Rashidi

*Author for correspondence: Tel.: +98 713 230 5291;

E-mail Address: sajaderashidi@yahoo.com

https://orcid.org/0000-0002-4675-7274

Department of Parasitology & Mycology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

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Published Online:17 May 2021https://doi.org/10.2217/fmb-2020-0303

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Abstract

Apolipoprotein A-I (apo A-I) represents the main component of the Trypanosome lytic factor (TLF) which contributes to the host innate immunity against Trypanosoma and Leishmania. These parasites use complex and multiple strategies such as molecular mimicry to evade or subvert the host immune system. Previous studies have highlighted the adaptation mechanisms of TLF-resistant Trypanosoma species. These data might support the hypothesis that Leishmania parasites (amastigote forms in macrophages) might express apo A-I to bypass and escape from TLF action as a component of the host innate immune responses. The anti-inflammatory property of apo A-I is another mechanism that supports our idea that apo A-I may play a role in Leishmania parasites allowing them to bypass the host innate immune system.

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Papers of special note have been highlighted as: • of interest

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Vol. 16, No. 8

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History

Received 2 December 2020

Accepted 9 April 2021

Published online 17 May 2021

Published in print May 2021

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Keywords

Author contributions

K Kalantar contributed toward conception, analysis, interpretation of data, drafting and revising, final approval and agreement for publication. R Manzano-Román contributed toward analysis, interpretation of data, drafting and revising, final approval and agreement for publication. E Ghani, R Mansouri and G Hatam contributed toward drafting and revising, final approval and agreement for publication. P Nguewa and S Rashidi contributed toward supervision, conception, analysis, interpretation of data, drafting and revising, final approval and agreement for publication.

Financial & competing interests disclosure

This work was supported by the National Institute for Medical Research Development (NIMAD), Tehran, Iran (grant number 963564). P Nguewa thanks Fundación La Caixa (LCF/PR/PR13/11080005), Fundación Caja Navarra, Gobierno de Navarra-Salud (12/2017), Fundación Roviralta, Ubesol, Government of Navarre, Laser Ebro, Inversiones Garcilaso de la Vega and COST Actions CA18217 (ENOVAT) and CA18218 for their support. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

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