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This blog was designed for the Biomedical Technology students at the Durban University of Technology, in Durban, South Africa. It consists of short notes on aspects that I feel that my students grapple with, and aims to provide a better explanation than that they would receive in lectures. It is also a very personal blog, where I feel comfortable 'talking' to my students.

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Wednesday, April 28, 2010

Effector functions of Antibodies

The principal reason for antibodies being produced is for agglutination. When the Ab combines with the Ag, it forms an immune complex. If the Ab is either IgG or IgM, the immune complex is capable of activating complement and results in lysis of the antigen.
However Ab serve many more functions. These are the effector functions referred to in the title. The Fc portion of the Ab can attach to many cells, and bring about a specific function. The function depends on the cell it attaches to. Some of the cells that can attach to the Fc portion are neutrophils, macrophages, monocytes and trophoblasts.
Not all Ab attach to these cells. The attachment is not really so. It is more an interaction via Fc receptors. These receptors are found on the surface of cells. The Ab that interact with Fc recptors are IgG, IgM, IgE. The Fc receptor is named according to the type of Ab it interacts with. It is Fc epsilon if it interacts with IgE, Fc gamma for IgG and Fc mu for IgM.

IgA is found in the various parts of the body where mucous is secreted. Many Ag enter the body here. The Ab interferes with colonization of the Ag and therefore reduces or stops infection taking place. The Ab also reduces the infectivity of viruses.
A toxin is produced by certain bacteria once they have entered the body. The toxin is harmful and can affect the body in many ways. The immune response is to both the Ag and the toxin. Ab produced in response to the toxin are specific to the toxin. Now the toxin exerts its effect by combining with man’s tissues/cells. The actual part that comes into contact with man’s tissues is called the active site. The immune system must somehow stop the active site from coming into contact with tissue. So the Ab does this in either one of two ways. Firstly the Ab will combine with the toxin near or actually at the active site. This effectively blocks the active site. Secondly the Ab combines far from the active site, thereby causing a change in the morphology or structure of the active site. In both instances, the active site is unable to carry out its function. A point to note here is that this is an example of active natural immunity. In the case of administration of antitoxin, it is passive artificial immunity.
I will deal with immune system compensation for non adherence to phagocyte in another blog entry

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