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. 2019 Oct 4;10:2265. doi: 10.3389/fimmu.2019.02265

Figure 2.

Figure 2

Periovular granuloma macrophages in schistosomiasis assume an M2-like phenotype with altered lipid metabolism. Antigens from Schistosoma mansoni eggs (and adults) activate PPAR-γ signaling. Some Schistosoma products have also been shown to inhibit signaling by the FAO inducer, PPAR-α. PPAR-γ contributes to an M2 phenotype by upregulating M2 markers including arginase-1. It also promotes expression of the scavenger receptor CD36, which takes up free fatty acids and oxidized LDL cholesterol. In contrast, PPAR-γ inhibits oxLDL cholesterol uptake via the LOX-1 receptor. S. mansoni itself also attenuates LOX-1 by decreasing ApoC1 and ApoC3 via an unknown mechanism. Additionally, S. mansoni infection also leads to an upregulation of CD14, which has in turn been shown to promote uptake of oxLDL and other lipids in macrophages. HDL cholesterol efflux may also be increased through the PPAR-γ-mediated upregulation of ABCA1 and ABCG1, contributing to an anti-atherogenic phenotype. Up- and downregulation are indicated by blue and red, respectively. ABC, adenosine triphosphate-binding cassette transporter; Apo, apolipoprotein; CD, cluster of differentiation; FAO, fatty acid oxidation; HDL, high-density lipoprotein; LOX-1, lectin-like oxidized low-density lipoprotein receptor 1; oxLDL, oxidized low-density lipoprotein; PPAR, peroxisome proliferator-activated receptor.