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. 2020 Jun 12;10(6):369. doi: 10.3390/brainsci10060369

Figure 2.

Figure 2

Central nervous system cells and Toxoplasma gondii. Tachyzoites from T. gondii can enter astrocytes, microglia and neurons. The presence of T. gondii induces functional changes in these cells which promote the release of anti- and pro-inflammatory cytokines, and alter both gliotransmission and neurotransmission. Neurons lack an effective defense system against the parasite, therefore, cysts with bradyzoites can form perpetuating the infection. In contrast, astrocytes and microglia possess different mechanisms to protect against the presence of tachyzoites. Abbreviations: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPA); Apolipoprotein E (APOE); C-X-C motif chemokine 10 (CXCL10); excitatory amino acid transporter (EAAT); γ-aminobutyric acid (GABA); guanylate-binding protein (GBP); immunity-related GTPases (IRG´s); indoleamine 2,3-dioxygenase (INO); Interleukin (IL); monocyte chemoattractant protein 1 (MCP-1); Macrophage Inflammatory Proteins 1 alpha (MIP-1α); nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); transforming growth factor beta (TGF-β).