File:The early immediate hypersensitivity phase of antigen-induced airway inflammation.jpg

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Revision as of 23:02, 1 May 2016 by Z5015719 (talk | contribs) (The IgE molecules bound to FceRI molecules on a single mast cell. The binding of IgE to FcεRI αβγγ on mast cells (located in airway tissue) up regulates FcεRI surface expression and causes these cells to respond when later exposed to specific ant...)
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The IgE molecules bound to FceRI molecules on a single mast cell. The binding of IgE to FcεRI αβγγ on mast cells (located in airway tissue) up regulates FcεRI surface expression and causes these cells to respond when later exposed to specific antigens. Furthermore, in mast cells, some IgE molecules can increase cytokine production and survival. Once FcεRI aggregation is induced through the recognition of antigens by at least two IgE molecules bound to adjacent FceRI molecules, mast cells become activated, leading to the initiation of an immediate hypersensitivity response. This involves the secretion of preformed mediators soon after antigen exposure. The mast cells further up regulate the production of many cytokines and growth factors. Minutes after exposure, the mediators lead to bronchoconstriction, vasodilatation and increased mucus production. Mast cell mediators can also contribute to late phase reaction by promoting an increase of circulating leukocytes, which can induce further inflammation and bronchoconstriction in the late phase of asthma.

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current23:02, 1 May 2016Thumbnail for version as of 23:02, 1 May 20161,050 × 881 (318 KB)Z5015719 (talk | contribs)The IgE molecules bound to FceRI molecules on a single mast cell. The binding of IgE to FcεRI αβγγ on mast cells (located in airway tissue) up regulates FcεRI surface expression and causes these cells to respond when later exposed to specific ant...
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