The IL-33/ST2 pathway is not essential to Th2 stimulation but is key for modulation and survival during chronic infection with Schistosoma mansoni in mice.

The IL-33/ST2 pathway is not essential to Th2 stimulation but is key for modulation and survival during chronic infection with Schistosoma mansoni in mice. Cytokine. 2020 Dec 16;138:155390 Authors: Maggi L, Rocha IC, Camelo GMA, Fernandes VR, Negrão-Corrêa D Abstract Morbidity during chronic schistosomiasis has been associated with the induction and modulation of type-2 granulomatous inflammatory response induced by antigens secreted by the eggs, which become trapped in capillary venules of the host tissues, especially in the liver and intestines. IL-33, an alarmin released after cell damage, binds to its ST2 (suppressor of tumorigenicity 2) receptor, expressed in an variety of immune cells, including ILC2 and macrophages, and stimulates the early production of IL-5 and IL-13, which leads to eosinophil infiltration and activation of a Th2 response. However, the role of IL-33/ST2 activation on Schistosoma-induced granuloma formation and modulation is mostly unknown. In the current work, we comparatively evaluated the immune response and granuloma formation in wild-type BALB/c (WT) and BALB/c mice genetically deficient in the IL-33 receptor (ST2-/-) experimentally infected with Schistosoma mansoni. Mice were infected with 25 or 50 S. mansoni cercariae and followed for up to 14 weeks to assess mortality. Mice from each experimental group were comparatively evaluated for parasite burden, liver immune response, and granuloma appearance...
Source: Cytokine - Category: Molecular Biology Authors: Tags: Cytokine Source Type: research