The Lab / Core medicine / Lesson 20
A germ slips in through a cut. Watch the body find it, raise the alarm, recognise it by its name tags, build an army made for that one invader and remember it for next time. Then watch four kinds of medicine steer the response up or down.
Educational, not for clinical use
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Your immune system is the body’s defence force. It wakes when a germ (or pathogen: a bacterium, virus or other tiny invader that causes disease) slips past the skin, say through a cut, and multiplies. That is an infection.
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Within hours, white blood cells, the body’s roaming defence cells, arrive. Macrophages and neutrophils are eating cells: they swallow germs whole and break them down. This fast, ready-made first defence, the same for every germ, is the innate response.
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Macrophages that meet germs send out alarm signals, tiny chemical messengers. A loud one is TNF (tumour necrosis factor). Nearby blood vessels widen and leak, letting in more eating cells. The redness, heat and swelling are inflammation (Lesson 18).
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Every germ carries surface shapes of its own, called antigens: name tags that mark it as foreign. Some eating cells carry a torn-off tag to a lymph node, a bean-shaped meeting place where the body’s specialist defenders wait.
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In the node wait T cells, white blood cells that each fit just one tag. When a helper T cell finds its tag, a switch inside flips: calcineurin, an enzyme (a tiny machine that does one job). It sends the signal: grow.
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The switched-on T cell copies itself again and again into a clone: a crowd of identical cells that all fit the same tag. This made-to-measure, slower second defence is the adaptive response. It takes days to build.
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B cells also fit just one tag. Helped by a matching helper T cell, a B cell turns into a plasma cell, a factory that pours out antibodies: Y-shaped grabbers whose two tips grip that one tag.
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Antibodies coat germs, clump them together and mark them for the eating cells. Killer T cells find body cells that a virus has taken over and destroy them, germ and all. Together they finish what the innate response could only hold back.
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Put it on a timeline. Germs climb at first while the innate response slows them and the alarm rings. The adaptive response takes days to build; once antibodies rise, the germs fall fast. Then the alarm quietens and most new cells die off.
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A few of the new T and B cells stay on for years as memory cells. If the same germ returns, they wake fast: antibodies rise sooner and higher, and the germ is beaten before it gets far. This is immunity.
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Germ in; eating cells and alarm signals first; tags to the node; T cells switch on and multiply; B cells make antibodies; memory stays. Key measures: how far the germs climb, and how many antibodies are made. Immune drugs steer the response at four points.
What changes it
A vaccine shows the body a germ’s tags, or a killed or weakened copy of the germ, without the illness. Memory cells form ahead of time, so when the real germ arrives, antibodies rise early and the germ never climbs far.
What changes it
Calcineurin inhibitors, such as tacrolimus and ciclosporin, block the T cell’s on switch. The grow signal stops, so few T cells multiply and B cells get little help. This stops the body attacking a transplant, a donated organ, but germs spread more easily.
What changes it
Anti-TNF biologics are lab-made molecules, grown in living cells, that grab and hold TNF; most are antibodies, some are decoy TNF catchers. Less alarm means less inflammation, calming diseases where the immune system attacks the joints or gut, but germs are held back less.
What changes it
Glucocorticoids are steroid drugs modelled on cortisol, the body’s own stress messenger (Lesson 15). They enter immune cells and turn down the instructions for many alarm signals at once. Inflammation falls and fewer T cells multiply, but germs are fought less well.
Start with Next, or use the arrow keys. Pictures are illustrative, not measurements. White blood cells meet bacteria in Lesson 19.
Loading reference values…
Normal teaching baseline.
The blue line on each bar, and the large number beside it, show where an illustrative teaching model sits: not a patient measurement and not a sourced value. The shaded bands are the reference ranges quoted under each row. The picture and every bar come from the same model. Selecting a condition applies it to the model, and the dashed line shows the model without it. Separately, an arrow labelled “Cited” appears only where the quoted source gives that row’s direction; where it does not, no arrow is shown and the marker is the teaching model alone. The source describes cell counts, so it can give a direction for the total count but not for the shares.
The source also describes infections, allergies and steroid drug therapy, but only as changes in the number of one kind of white cell. It gives no reference range for those numbers and no direction for the total or the shares shown above, so these are quoted here instead of being offered as conditions with arrows. Try them on the model with the infection, germ and drug controls; what the model shows is illustrative.
Vaccines, calcineurin inhibitors and anti-TNF biologics are animated in the Lesson and in Explore freely, and the drug control above applies an illustrative effect to the model. They are not listed as states, with arrows, because the reference used on this tab gives no direction for any of them on these values, and every state here must quote its source.
An illustrative teaching model of one infection and the immune response to it. Set how fast the germ multiplies, add a vaccine or immune drugs (they combine) and watch the germs, alarm signals, T cells and antibodies over time. Dashed marks are the untreated, unvaccinated response, this lesson’s normal; solid marks are your settings.
Germs multiply toward a ceiling at the site. Eating cells kill a few, and more of them arrive when alarm signals are active. Alarm signals are made while germs are present and fade quickly. T cells that fit the germ’s tag multiply while the tag is around, helped a little by the alarm; plasma cells make antibodies with T cell help; antibodies and T cells kill germs. Memory cells build up during the response, wake at far smaller amounts of the tag, and quickly make many antibody factories.
A vaccine starts the run with memory cells and a few antibodies already present. A calcineurin inhibitor mostly blocks the T cells’ on switch, which also starves B cells of help. An anti-TNF biologic removes most of the active alarm signal, so fewer eating cells arrive. A glucocorticoid lowers how much alarm signal is made and halves T cell switching on. The bars show how high each measure climbs during the first infection (memory: what is left at its end), relative to the untreated, unvaccinated response.
Left out: the many kinds of alarm signal, antibody and white blood cell; fever; the lymph and blood traffic between tissue and node; how drugs are absorbed and cleared (Lesson 17); side effects; every difference between germs and between people. Nothing here predicts a real infection, and nothing here is a treatment plan.