SNPs in toll-like receptor (TLR) genes as new genetic alterations associated with congenital toxoplasmosis?

Nearly 40 % of pregnant women are infected with Toxoplasma gondii. Primary infections in pregnant women result, in approximately 30–50 % of patients, in transmission of T. gondii through the placenta to the fetus and then in congenital infections with severe, sometimes fatal course. Studies still do not provide sufficient data on the genetic bases of the immunity in fetuses, newborns, and infants with congenital toxoplasmosis. Previous research showed the contribution of toll-like receptors (TLRs) to non-specific immunity against T. gondii invasion, observed in T. gondii-infected animals, especially mice. So far, the activity of TLRs in defense against T. gondii infections was observed particularly for TLR2, TLR4, and TLR9 molecules. Differential TLR activity associates with both cell types, including a variety of placental cells and stage of pregnancy. Several single-nucleotide polymorphisms (SNPs) residing in three genes encoding these receptors were reported as significant genetic modifications of TLRs associated with different pregnancy disorders. Despite those data, genetic alterations of TLRs which have contributed to innate immune response against T. gondii infections are still not precisely described. In this article, we present reasons for the research of the plausible role of SNPs residing in TLR2, TLR4, and TLR9 genes in congenital toxoplasmosis development.