**5.3 Taeniasis**

*Toll-like Receptors*

**5.2 Schistosomiasis**

TNFα production [101] (**Figure 6**).

asymptomatic infection in initial stages but leads to secondary infection by bacteria and virus in filarial patients [92]. A phosphocholine-containing glycoprotein (ES-62) of *Acanthocheilonema viteae* (rodent filarial nematode) inhibits B and T lymphocyte activation. The secretory ES-62 inhibits TLR4-mediated IL-12 and

Schistosomiasis is a worldwide distributed parasitic disease caused by a flatworm, Schistosoma. It accounts for 260 million infected people in tropical and sub-tropical regions (Africa, South America, the Middle East, East Asia, and the Philippines) [102]. *S. mansoni*, *S. intercalatum*, *S. haematobium*, *S. japonicum,* and *S. mekongi* are the five species of schistosomes that cause disease in humans. *S. mansoni*, *S. japonicum,* and *S. intercalatum* are responsible for intestinal schistosomiasis, while *S. haematobium* causes urinary schistosomiasis and is most important in terms of public health [102]. Fresh water snail of the genus *Bulinus* (*S. haematobium*), *Biomphalaria* (*S. mansoni*), and *Oncomelania* (*S. japonicum*)

*S. japonicum* eggs are deposited in the liver, lung, and intestinal wall of host, which induce granulomatous inflammation and progressive fibrosis. Th cells, natural killer (NK) cells, NKT cells, myeloid-derived suppressor cells (MDSCs), and macrophages are mainly involved in fight against *S. japonicum* and its eggs [104]. Expressions of TLR1, TLR3, TLR7, TLR8, and NF-κB are greatly repressed at the initial stage of schistosomiasis. TLR3 modulates Th2 response in lung in *S. mansoni* infection and in NK cells during *S. japonica* infection [105]. *S. mansoni* is known to attenuate Th1 responses (decrease IFN, TNF, IL-12, and NO) but to promote Th2 immune responses (increase IL-10 and TGF) [106]. Although TLR4 protects the host from Schistosoma infection, TLR2 favors the parasite growth [107]. Both SEA (soluble egg antigen) and ES products of *S. mansoni* act as a strong inducer of Th2 response [108]. It induces transcription of markers CD40 and CD86 and cytokines IFNβ, TNFα, and IL-12-p40 in mouse myeloid DCs [109]. Glycans present in *S. mansoni* induce Treg by TLR2-mediated DC differentiation and IL-10 secretion [110]. Schistosoma egg product LFNP III also stimulates IL-10 production

acts as an intermediate host of Schistosoma parasites [103].

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**Figure 6.**

*TLR signaling pathway induced by Helminth pathogens.*

The pork tapeworm (*Taenia solium*) is a cestoda parasite transmitted to humans by feeding cystic larvae infected pork. Here, pig acts as an intermediate host, which swallows *T. solium* egg containing human stool and develops larva inside their body [114]. The cysticercosis cyst causes neurocysticercosis (NCC) in the nervous system, and adult taenia produces intestinal taeniasis in humans. Both are endemic in Latin America, sub-Saharan Africa, India, vast parts of China, and South East Asia [115].

TLR4 and TLR2 play an important role in developing murine NCC caused by *Mesocestoides corti* [116]. The carbohydrate of *T. crassiceps* induces TLR4- and TLR2-mediated cytokine release (IL-6 and IL-4) [117]. However, molecules derived from *T. sodium* did not induce TLR2- or TLR4-mediated cytokine release in human lymphocytes [118]. Both *T. solium* and *T. crassiceps* express several glycolipids (GSL-1) and phospholipids that may act as PAMPs. *T. crassiceps* expresses lysophosphatidylcholine [119], also present on Schistosome, and triggers TLR2 response. Although the mechanism of these molecules inducing TLR signaling has not yet been evaluated, the host may use a similar pathway of this parasite recognition [120] (**Figure 6**).
