11c - immunity

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1 2 3 4 5 1. Macrophage performs phagocytosis on the incoming bacteria. They break down the body of the pathogen except for its antigen, which the macrophage will use to display upon their cell surface membrane. This is called antigen presenting mechanism, to display a specific antigen on the cell surface membrane so that it can be recognized by another cell. 2. T-helper (immature) come from a specific precursor T-lymphocyte from the thymus gland. This precursor T-lymphocyte, takes in a specific antigen and becomes activated. They will divide to make 3 subtypes of T cells; T-helper cells (activate B cells), T-cytotoxic cell (become T-killer cells) and T-suppressor cell (you don't effing need to know). This T-helper cell carries a receptor that is specific to one antigen which the precursor T-lymphocyte was activated to earlier. Remember, at this stage, the T-helpers are not ready to divide yet until they are activated by the macrophage. 3. Remember the macrophage earlier has displayed the right antigen on its surface? Now the T-helper also carries the receptor that recognizes the same antigen as well. So now what happens? The T-helper and the macrophage will bind to each other because their receptors are compatible to each other. Once they bind, macrophages will release cytokines to the T- helper cells so that they will become activated. Once they are activated the outcome will be; a) All T-helper cells will divide rapidly by mitosis b) All the clone T-helper cells will be specific to one antigen only Now these activated T-helper cells can do the following; a) Activate B cells b) Secrete cytokines to stimulate macrophages to induce more phagocytosis. 4. The B-lymphocytes at this time are immature, means they are not ready to divide by mitosis yet. But what they can do is to ingest a specific antigen and their receptors become specific to one antigen. Now the activated T-helper cells can bind to these B-lymphocytes because their receptors are specific to the same antigen. But once they bind, the T-helper cells can release cytokines to the B-lymphocytes and activate them. Once they are activated the outcome will be; a) All B-lymphocytes cells will divide rapidly by mitosis b) All the clone B-lymphocyte cells will be specific to one antigen only 5. Now the B-lymphocytes will divide rapidly and create more clones. Their clones are divided to two groups basically. They are the B-memory cells and the plasma cells. The plasma cells will secretes specific antibodies that target one antigen.

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Page 1: 11C - Immunity

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1. Macrophage performs phagocytosis on the incoming bacteria. They break down the body of the pathogen except for its antigen, which the macrophage will use to display upon their cell surface membrane. This is called antigen presenting mechanism, to display a specific antigen on the cell surface membrane so that it can be recognized by another cell.

2. T-helper (immature) come from a specific precursor T-lymphocyte from the thymus gland. This precursor T-lymphocyte, takes in a specific antigen and becomes activated. They will divide to make 3 subtypes of T cells; T-helper cells (activate B cells), T-cytotoxic cell (become T-killer cells) and T-suppressor cell (you don't effing need to know). This T-helper cell carries a receptor that is specific to one antigen which the precursor T-lymphocyte was activated to earlier. Remember, at this stage, the T-helpers are not ready to divide yet until they are activated by the macrophage.

3. Remember the macrophage earlier has displayed the right antigen on its surface? Now the T-helper also carries the receptor that recognizes the same antigen as well. So now what happens? The T-helper and the macrophage will bind to each other because their receptors are compatible to each other. Once they bind, macrophages will release cytokines to the T-helper cells so that they will become activated. Once they are activated the outcome will be;

a) All T-helper cells will divide rapidly by mitosis b) All the clone T-helper cells will be specific to one antigen only

Now these activated T-helper cells can do the following;a) Activate B cellsb) Secrete cytokines to stimulate macrophages to induce more phagocytosis.

4. The B-lymphocytes at this time are immature, means they are not ready to divide by mitosis yet. But what they can do is to ingest a specific antigen and their receptors become specific to one antigen. Now the activated T-helper cells can bind to these B-lymphocytes because their receptors are specific to the same antigen. But once they bind, the T-helper cells can release cytokines to the B-lymphocytes and activate them. Once they are activated the outcome will be;

a) All B-lymphocytes cells will divide rapidly by mitosis b) All the clone B-lymphocyte cells will be specific to one antigen only

5. Now the B-lymphocytes will divide rapidly and create more clones. Their clones are divided to two groups basically. They are the B-memory cells and the plasma cells. The plasma cells will secretes specific antibodies that target one antigen.

Page 2: 11C - Immunity
Page 3: 11C - Immunity

The significance of white blood cell counts

A normal white blood cell count is between 4500 to 10 000 cells per µl, but during active

infections in the body the number rises and may be considerably higher. Given the roles of

white blood cells when in the presence of pathogens within the body, this relationship is of

no surprise. Another cause of raised white blood cell count is leukaemia – a cancer of the

bone marrow cells. The stem cells from which white blood cells are normally formed

proliferate but fail to differentiate. Here the numbers can be very high indeed, but a variety

of abnormal cells present.

Myasthenia gravis – a failure to distinguish ‘self’ from

‘non-self’

Myasthenia gravis is an usual auto-immune disorder in which specific antibodies attack and

destroy the acetylcholine receptors at the post-synaptic junctions, thereby inhibiting the

effect of the neurotransmitter acetylcholine (Chapter 15). This disease is one of the less

common auto-immune disorders, affecting about two people in every 10 000 of the

population. It causes muscle weakness. The effects of the disease may be localised in the

body, involving just the eye muscles for example. Alternatively, many muscle systems may

be affected, leaving the sufferer susceptible to general fatigue. In the presence of this

condition, muscles weaken during periods of activity but improve with resting. Some

patients with myasthenia gravis are found to have a tumour of the thymus gland. These are

often benign, but the gland is then removed as a precaution, and typically symptoms of

myasthenia gravis improve.