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Review
. 2018 Oct 31:9:2529.
doi: 10.3389/fimmu.2018.02529. eCollection 2018.

Macrophage Polarization in Leishmaniasis: Broadening Horizons

Affiliations
Review

Macrophage Polarization in Leishmaniasis: Broadening Horizons

Fernanda Tomiotto-Pellissier et al. Front Immunol. .

Abstract

Leishmaniasis is a vector-borne neglected tropical disease that affects more than 700,000 people annually. Leishmania parasites cause the disease, and different species trigger a distinct immune response and clinical manifestations. Macrophages are the final host cells for the proliferation of Leishmania parasites, and these cells are the key to a controlled or exacerbated response that culminates in clinical manifestations. M1 and M2 are the two main macrophage phenotypes. M1 is a pro-inflammatory subtype with microbicidal properties, and M2, or alternatively activated, is an anti-inflammatory/regulatory subtype that is related to inflammation resolution and tissue repair. The present review elucidates the roles of M1 and M2 polarization in leishmaniasis and highlights the role of the salivary components of the vector and the action of the parasite in the macrophage plasticity.

Keywords: Leishmania; chemokine; classical macrophage; immunomodulation; non-classical macrophage; vector saliva.

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Figures

Figure 1
Figure 1
Role of saliva vectors on macrophage polarization. Vector saliva induces the recruitment of neutrophils and macrophages and acts as an immunomodulator to reduce pro-inflammatory and microbicidal molecules and improve Th2 cytokines and regulatory molecules, which lead to a M2 polarization. M2 macrophages allow for the facilitated entry of Leishmania promastigotes and higher survival/proliferation of intracellular amastigotes.
Figure 2
Figure 2
Role of M1 and M2 macrophages in Leishmania infection. TACI (transmembrane activator and calcium modulator and cyclophilin ligand interactor), peroxisome proliferator-activated receptors (PPARs) and mesenchymal stem cells (MSCs) participate in M1 polarization in macrophage-leishmania studies, as well as the crotoxin treatment. The epithelial and myeloid-derived serine protease inhibitor (SLPI), mammalian target of rapamycin (m-TOR) and the treatment with high diluted antimony participate in M2 polarization in leishmania models.

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