B-cells are responsible for humoral immunity. They arise from a separate population of stem cells of the bone marrow than that which gives rise to T-cells. These cells undergo multiplication and processing in lymphoid tissue elsewhere than in the thymus gland. In birds, the lymphoid tissue concerned has been located in the gut and called the bursa of Fabricius.
In humans, the site is unknown although there is some evidence to suggest that such processing occurs in the bone marrow itself or in the foetal liver.
Lymphocytes processed in this way are called B-lymphocytes after the bursa.
B-cells, like T-cells, have surface
receptors which enable them to recognise the appropriate antigen, but do not themselves
interact to neutralise or destroy the antigen. On recognition of the antigen they take up
residence in secondary lymphoid tissue and proliferate to form daughter lymphocytes,
processed in the same way as themselves. These B-cells
then develop into short-lived plasma cells.
The plasma cells produce antibodies and release them into the circulation at the lymph
nodes.
Some of the activated B-cells do not become plasma cells instead they turn into memory
cells which continue to produce small amounts of the antibody long after the infection has
been overcome.
As with T-cells millions of B-cells are
produced each with a different antigen binding specificity
If the B-cell comes into contact with the specific type of antigen to which it is targeted
it divides rapidly to form a clone of identical cells.
This antibody circulates as part of the gamma globulin
fraction of the blood plasma.
Should the same antigen enter the body again this circulating antibody acts quickly to
destroy it.
At the same time memory cells quickly divide to produce new clones of the appropriate type
of plasma cell.
Antibodies are Y shaped molecules.
They have binding sites for specific antigens.
There are 5 classes of antibodies (although each class has many variations). Each is called an immunoglobulin and then allocated a code letter. However conventionally they are normally written as IgA with the Ig standing for immunoglobulin. Thus IgA stands for immunoglobulin A.
IgA about 15% of total antibody count. Found in mucous secretions of the respiratory tract and the upper part of the digestive tract and the vagina. Also found in colostrum. Colostrum is a golden liquidy substance that a nursing mother expels from her breasts 24-48 hours after delivery. This substance is produced before the milk and is very important in the transfer of antibodies to a newborn infant. IgA given by the mother in the colostrum will protect the baby for about six months. Note IgA has two binding sites as shown diagrammatically below.

IgD less than 1%
Appears to have a role in activating and suppressing lymphocyte activity
Found in large quantities in the cell walls of many B-cells. IgD has a single binding
site.

IgE less than 1%
Mediator in allergic responses. Most importantly activates histamine secreting cells. Also
appears to play a role in parasitic infection. IgE has a single binding site.

IgG- composes 75% of our immunoglobulin pool. IgG stimulates phagocytic cells, activates the complement system, binds neutrophils, and can neutralise toxins. Most importantly, it is the only antibody that can cross the placenta and confer immunity on the foetus. IgG also has a single binding site.

IgM - makes up 10% of our total antibodies. This is the predominant early antibody; the one that first activates in an initial attack of antigen. Because of its high number of antigen binding sites (5), it is an effective agglutinator of antigen . This is important in the initial activation of B-cells, macrophages, and the complement system.
When floating freely in body fluids the IgM molecule
assumes a star shape as shown on the left. However when it attacks a foreign body the five
arms can assume a 'crab-like' appearance with all five binding sites attached to the
surface of the invading organism.
Related links
[ The Lymphatic System ] [ The Blood ] [ Introduction to Microbiology ] [ Non-specific Innate Defences ]
Web Page authored by John Ross
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This page last updated on Friday, 09 July 1999 13:46 +0100