Table 3.
STATs in helminth infections
| Parasite | Effect | References | |
|---|---|---|---|
| STAT1 | Schistosoma mansoni | Soluble egg antigens (SEA) do not induce STAT1 phosphorylation in macrophages but induce ERK and p38 activation. | 30 |
| STAT4 | Taenia crassiceps | Genetically resistant C57BL/6 mice became susceptible when lacking STAT4 gene. | 34 |
| Setaria digitata | Secreted filarial lipids (SFL) down-regulate Th1 immune responses by decreasing STAT4 phosphorylation in a dose-dependent manner. | 35 | |
| Nippostrongylus brasiliensis | Decrease in frequency of IL-4 producing cells in infected STAT4-/-mice. | 36 | |
| STAT6 | Nippostrongylus brasiliensis | IL4-Rα and STAT6 are necessaries for worm expulsion; IL-13 is decisive for clearance. | 4 |
| Trichinella spiralis | Absence of STAT6 is related to higher parasite burden and lower Th2 cytokines. | 50 | |
| STAT6 and Th2 cytokines seems to be necessary for goblet cell hyperplasia. | 51 | ||
| Gut muscle hyper-contractility necessary for worm expulsion depends on STAT6 signaling. | 56 | ||
| Hymenolepis diminuta | Resistance is mediated by STAT6 but do not depend on IL-4 or IL-13 alone. The absence of STAT6 down regulates goblet cells. | 61 | |
| Brugia malayi | IL-4 and STAT6 are required for clearance from BALB/c and C57BL/6 mice. | 63 | |
| Taenia crassiceps | STAT6 deficient mice were resistant to infection with an intense Th1 response. | 65 | |
| Mesocestoides corti | In murine neurocysticercosis STAT6 deficient mice succumbed faster given an intense inflammatory response | 67 |