Difference between revisions of "File:The early immediate hypersensitivity phase of antigen-induced airway inflammation.jpg"

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(Role of mast cells in asthma)
(Role of mast cells in asthma)
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==Role of mast cells in asthma==  
 
==Role of mast cells in asthma==  
 
===Original Image legend===
 
 
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.
 
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.
  
 
===Reference===
 
===Reference===
PMID 3597223
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PMC3597223
  
<pubmed> 3597223 </pubmed>
+
<pubmed> PMC3597223 </pubmed>
  
 
===Copyright===
 
===Copyright===
Copyright Urb, Sheppard. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
+
This page has information about general copyright restrictions that apply to the material that is available through the PubMed Central (PMC) site. There also are links to some Publisher Specific Copyright Information.
 +
 
 +
All of the material available from the PMC site is provided by the respective publishers or authors. Almost all of it is protected by U.S. and/or foreign copyright laws, even though PMC provides free access to it. (See Public Domain Material below, for one exception.) The respective copyright holders retain rights for reproduction, redistribution and reuse. Users of PMC are directly and solely responsible for compliance with copyright restrictions and are expected to adhere to the terms and conditions defined by the copyright holder. Transmission, reproduction, or reuse of protected material, beyond that allowed by the fair use principles of the copyright laws, requires the written permission of the copyright owners. U.S. fair use guidelines are available from the Copyright Office at the Library of Congress.
  
 
{{Student Image}}
 
{{Student Image}}

Revision as of 23:06, 1 May 2016

Role of mast cells in asthma

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.

Reference

PMC3597223

<pubmed> PMC3597223 </pubmed>

Copyright

This page has information about general copyright restrictions that apply to the material that is available through the PubMed Central (PMC) site. There also are links to some Publisher Specific Copyright Information.

All of the material available from the PMC site is provided by the respective publishers or authors. Almost all of it is protected by U.S. and/or foreign copyright laws, even though PMC provides free access to it. (See Public Domain Material below, for one exception.) The respective copyright holders retain rights for reproduction, redistribution and reuse. Users of PMC are directly and solely responsible for compliance with copyright restrictions and are expected to adhere to the terms and conditions defined by the copyright holder. Transmission, reproduction, or reuse of protected material, beyond that allowed by the fair use principles of the copyright laws, requires the written permission of the copyright owners. U.S. fair use guidelines are available from the Copyright Office at the Library of Congress.

Note - This image was originally uploaded as part of a student project and may contain inaccuracies in either description or acknowledgements. Please contact the site coordinator if the uploaded content does not meet the original copyright permission or requirements, for immediate removal.

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