Il-33 For Inflammatory Response in Immune Cells - 7 Angebote vergleichen

Lieferung aus: Deutschland, zzgl. Versandkosten.
Interleukin-33 belongs to Interleukin-1 cytokine family, primarily exuded by disrupted epithelial cells (ECs) and it functions as "alarmin". Numerous structural cells namely epithelial cells, keratinocytes, fibroblasts and endothelial cells expresses IL-33. Lately, IL-33 is recognised as a distinct ligand for ST2 receptor, primarily expressed on various hematopoietic cells viz. mast cells, type 2 T-helper cells, eosinophils, ILC2s and basophils. IL-33 forms hetero-dimer by binding to the ST2L and Interleukin-1 receptor accessory protein. Receptor complex of Intracellular TIR domain phosphorylates and recruits several adaptor molecules involving MyD88, IRAK1, IRAK4, and TRAF6 which activate downstream NF-¿B, p38, JNK and ERK signalling pathways, results in inflammatory mediators production i.e. IL-1¿, TNF-¿, IL-13 etc. IL-33 has a pivotal role in adaptive as well as immune response by inducing Th2 mediated immune response. Asthma is an inflammatory disorder characterised by classical features such increased Th2 cytokine production which results in reversible airflow obstruction, hyperresponsiveness of the airways and mucous overproduction. Mast cells are immune cells which are located underneath epithelial cells and these cells are primary effector cells in asthma pathogenesis. ST2 receptor is immensely present on mast cells and cell activation is when IL-33 binds to the receptor. In response to IL-33 binding, these cells secrete Th2 cytokines, hence contributes in asthma development. Airway smooth muscle provides the required microenvironment for the mast cells to differentiate, activate, and survive. Various products of mast cells are capable to adversely affect the growth as well as functioning of smooth muscle and mast cells microlocalization in smooth muscle possibly prompt this interaction, hence resulting in amplified response. Bronchial epithelial cells have a key function in inducing, enhancing and regulating inflammation in the airways. MCs accumulation in airway epithelium is a prominent characteristic of the deranged mucosal physiology in disease associated allergy. When bronchial epithelial cells interact with mast cells, it produces IL-6, CXCL8 and CXCL1 via activation of NF-¿B and MAPK signalling pathways in airway inflammation.

Lieferung aus: Vereinigte Staaten von Amerika, Versandkosten nach: USA.
Von Händler/Antiquariat, Creative Centers.
A.K. Publications. paperback. New.

Von Händler/Antiquariat, AHA-BUCH GmbH [51283250], Einbeck, Germany.
nach der Bestellung gedruckt Neuware 88 pp. Englisch, Books.

Von Händler/Antiquariat, Chiron Media [55661942], Wallingford, United Kingdom.
Books.

Von Händler/Antiquariat, CreativeCenters [60598963], Peoria, IL, U.S.A.
Books.

Lieferung aus: Vereinigte Staaten von Amerika, zzgl. Versandkosten, Versandgebiet: DOM.
Von Händler/Antiquariat, Awesomebooks_Newbooks, DE, Wilmington, [RE:4].
PF.

Lieferung aus: Vereinigtes Königreich Großbritannien und Nordirland, zzgl. Versandkosten, Versandgebiet: EUR.
Von Händler/Antiquariat, Revaluation Books, DEVON, Exeter, [RE:3].
Trade paperback.