
Infection with helminth parasites poses a significant challenge to the mammalian immune system. The type 2 immune response to helminth infection is critical in limiting worm-induced tissue damage and expelling parasites. Conversely, aberrant type 2 inflammation can cause debilitating allergic disease. Recent studies have revealed that key type 2 inflammation-associated immune and epithelial cell types respond to Notch signaling, broadly regulating gene expression programs in cell development and function. Here, we discuss new advances demonstrating that Notch is active in the development, recruitment, localization, and cytokine production of immune and epithelial effector cells during type 2 inflammation. Understanding how Notch signaling controls type 2 inflammatory processes could inform the development of Notch pathway modulators to treat helminth infections and allergies.
Receptors, Notch, Helminthiasis, Epithelial Cells, Dendritic Cells, Immunity, Innate, Host-Parasite Interactions, T-Lymphocyte Subsets, Helminths, Leukocytes, Animals, Humans, Lymphocytes, Signal Transduction
Receptors, Notch, Helminthiasis, Epithelial Cells, Dendritic Cells, Immunity, Innate, Host-Parasite Interactions, T-Lymphocyte Subsets, Helminths, Leukocytes, Animals, Humans, Lymphocytes, Signal Transduction
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