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Several physiological and immunulogical systems and mediators are involved into the pathogenesis of hereditary angioedema. This list contains links to background information about these systems and their critical components. It is frequently updated. Please send us your comments or
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Physiological systems involved
Systems involved in the pathogenesis of hereditary angioedema
Wikipedia entry: Complement system
Public domain internet encyclopaedia
Wikipedia [3/08]: The complement system consists of a number of small proteins found in the blood, normally circulating as inactive zymogens. When stimulated by one of several triggers, proteases in the system cleave specific proteins to release cytokines and initiate an amplifying cascade of further cleavages. The end result of this activation cascade is massive amplification of the response and activation of the cell-killing membrane attack complex. Over 20 proteins and protein fragments make up the complement system, including serum proteins, serosal proteins, and cell membrane receptors. These proteins are synthesized mainly in the liver, and they account for about 5% of the globulin fraction of blood serum.
Full Wikipedia entry: Complement system
Wikipedia entry: Kinin-kallikrein system
Public domain internet encyclopaedia
Wikipedia [3/08]: The kinin-kallikrein system or simply kinin system is a poorly delineated system of blood proteins that plays a role in inflammation, blood pressure control, coagulation and pain. Its important mediators bradykinin and kallidin are vasodilators and act on many cell types.
Full Wikipedia entry: Kinin-Kallikrein-System
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Author: Jerini AG
Source: HAE-Network Status: 3/08 This list is frequently updated. Please send us your comments or suggestions by e-mail. |
