Let's take an example: there is a bacterium in a intestine tube. It, then, goes and attacks one cell of the intestine tube. After killing that cell, it keeps there attacking the others cells nearby.
"Who" is the first immune system agent to find that bacterium?
Did "he" get there randomly, by accident? Or was "he" sent there?
If sent, who sent/called it?
What does "he" do as soon as he "sees" the bacterium killing the cells?
Any brief explanation is appreciated.
"Who" is the first immune system agent to find that bacterium?
Did "he" get there randomly, by accident? Or was "he" sent there?
If sent, who sent/called it?
What does "he" do as soon as he "sees" the bacterium killing the cells?
Any brief explanation is appreciated.
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So in a lot of cases bacteria enter the system via cuts and grazes, where they encounter macrophages that are resident in the tissue. These macrophages recognise the pathogen as an enemy and phagocytose them, presenting the antigen on the surface of the cell. This will probably happen in hundreds or thousands of macrophages. Eventually, the t helper cell with the antigen receptor complementary to the shape of the antigen comes into contact with the macrophage APC in the lymphatic system (which is where most lymphocytes are found) and the t helper cell binds to the antigen, proliferates, releases cytokines and is able to then bind to other antigens. Meanwhile, if any of the pathogens have found their way into the blood or lymphatic systems and met the B lymphocyte with the antigen receptor complimentary to the shape of that antigen (just out of chance) they'll be ingested and processed and the B cell will become an APC. Then the t helper cell will bind to the antigen on the B cell, release cytokines and cause it to proliferate too- this leads to antibody production.
Also, in the site of infection (e.g. the skin) a body cell can also become an APC if it gets infected. This can then be bound to by the t killer cell with the antigen binding site specific to that of the antigen. An active t helper cell releases cytokines and this allows the t killer cell to become activate, proliferate and then to kill the infected cell by releasing perforins.
Also, in the site of infection (e.g. the skin) a body cell can also become an APC if it gets infected. This can then be bound to by the t killer cell with the antigen binding site specific to that of the antigen. An active t helper cell releases cytokines and this allows the t killer cell to become activate, proliferate and then to kill the infected cell by releasing perforins.
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