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Publisher plus sign by my mouse9/4/2023 We initially described IL-33 as an NF abundantly expressed in high endothelial venules (HEVs), specialized blood vessels mediating lymphocyte recruitment into lymph nodes ( 1). An important role for IL-33 in innate, rather than acquired, immunity is also supported by observations in IL-33–deficient mice ( 18). These innate immune cell populations have been shown to respond to IL-33 by producing extremely high amounts of the Th2 cytokines IL-5 and IL-13 ( 13– 16), as well as to play important roles in innate immune responses after helminth infection in the intestine ( 13, 15, 16) or influenza virus infection in the lungs ( 14, 17). IL-33 is also a potent activator of type 2 innate immune cell populations that have been described recently, including natural helper cells from adipose tissues and lung ( 13, 14), nuocytes from mesenteric lymph nodes and spleen ( 15), and innate helper 2 cells from various tissues ( 16). Interleukin-33 (previously known as NF from high endothelial venules) ( 1, 2) is an IL-1–like cytokine that signals through the ST2 receptor ( 3) and drives production of cytokines and chemokines in target cells ( 4, 5), including mast cells ( 6– 8), basophils and eosinophils ( 9), endothelial cells ( 10), Th2 lymphocytes ( 3), and invariant NKT and NK cells ( 11, 12). Together, our findings support the possibility that IL-33 may function as a nuclear alarmin to alert the innate immune system after injury or infection in epithelial barrier tissues. Finally, strong expression of the Il-33–LacZ reporter was also observed in inflamed tissues, in the liver during LPS-induced endotoxin shock, and in the lung alveoli during papain-induced allergic airway inflammation. Importantly, IL-33 protein was always localized in the nucleus of producing cells with no evidence for cytoplasmic localization. Constitutive expression of IL-33 was not detected in blood vessels, revealing the existence of species-specific differences between humans and mice. Immunostaining with anti–IL-33 Abs, using Il-33 Gt/Gt ( Il-33–deficient) mice as control, revealed that endogenous IL-33 protein is highly expressed in mouse epithelial barrier tissues, including stratified squamous epithelia from vagina and skin, as well as cuboidal epithelium from lung, stomach, and salivary gland. We found that the Il-33 promoter exhibits constitutive activity in mouse lymphoid organs, epithelial barrier tissues, brain, and embryos. In this study, we generated an Il-33–LacZ gene trap reporter strain ( Il-33 Gt/Gt) and used this novel tool to analyze expression of endogenous IL-33 in vivo. Little is known about endogenous IL-33 for instance, the cellular sources of IL-33 in mouse tissues have not yet been defined. IL-33 (previously known as NF from high endothelial venules) is an IL-1 family cytokine that signals through the ST2 receptor and drives cytokine production in mast cells, basophils, eosinophils, invariant NKT and NK cells, Th2 lymphocytes, and type 2 innate immune cells (natural helper cells, nuocytes, and innate helper 2 cells).
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