Evasion strategy Consequence(s) Molecular mechanism(s) Parasite effect References
Induction of IL-10 Decreased TH1 response;
Deactivation of macrophages
Independent of PGE2 Indirect Indirect [218,219]
Induction of TGF-β Reduced TNF-α production by macrophages;
reduced IFN-γ production by NK cells
Antagonizes IL-12 Indirect [130,220,221]
IFN-γ/-β upregulation Reduced IFN-γ levels and splenocyte proliferation   Indirect [222]
Inhibition of TNF- α
and IL-12 production
Deactivation of macrophages;
inhibition of TH1 responses
Reduced phosphorylation of p65/RelA; defective nuclear import of NF-kB; IL-10-independent STAT3 phosphorylation Direct [15,223-226]
Decreased IL-12 production by DCs Inhibition of TH1 responses LXA4-mediated downregulation
of CCR5
Indirect [227,228]
Blockade of MHC
class II upregulation
Defective antigen presentation to CD4+ T cells Reduced activity of CIITA and IRF-1 promoters Direct [56,229]
Inhibition of NO production Defective antiparasitic activity Inhibition of iNOS transcription Direct [194,195]
Inhibition of NO production in microglia Reduced antiparasitic activity Secretion of PGE2,
IL-10 and TGF-β
Indirect [230,231]
Inhibition of p47 GTPases   Reduced transcription   [232]
Significant suppression of IL-2, IFN-γ (but not IL-10). Markedly lower levels of IgG1, IgG2a, IgG2b, IgG3, IgA, IgM Suppressed cytokine and immunoglobulin secretions by murine splenic lymphocytes   Indirect [21]
CIITA: Master Regulator of Major Histocompatibility Complex Class II Transcription; CCR5: CC Chemokine Receptor; DCs: Dendritic Cells; iNOS: Inducible Nitric Oxide Synthase; IRF-1: Interferon Regulatory Factor-1; LXA: Lipoxin A4; MHC: Major Histocompatibility Complex Molecules; PGE2: Prostaglandin E2; TGF-β: Transforming Growth Factor-β. Proliferation of T . gondii in inflammatory macrophages was associated with diminished ROS production in host cells [233]. In young children with congenital toxoplasmosis specific T cell response to the parasite antigens was impaired and such hyporesponsiveness has been restored during childhood. The acquisition of functional T cell response was disease-unrelated and indistinguishable
in terms of strength, epitope specificity, and cytokine profile from the corresponding responses in immunocompetent adults with asymptomatic acquired T. gondii infection [234].
In pregnant mice, T. gondii infection caused a decrease of CD4+CD25+-regulatory T cells [235]. It must be noted that peripheral blood leukocytes (PBL) from healthy children older than 36 mths responded to several stimuli at levels comparable to those of PBL from adults, but surprisingly, cord blood leukocytes appeared to be more efficient in antigen-presenting function than PBL from children younger than 13 months [236].
Table 9: Partial downregulation of cell-mediated immune responses after infection with T. gondii (Lang, Gro & Lüder [217]; with own modification).