Your blood holds millions of different lymphocytes, each with receptors of one shape. An infection is beaten when the few that fit the invader are found and cloned, and the second time it is far quicker.
In a primary immune response a macrophage engulfs a pathogen and presents its antigens. The one T-helper cell with complementary receptors binds (clonal selection) and divides by mitosis (clonal expansion); its clones release cytokines. The B-lymphocyte with complementary receptors, stimulated by cytokines, divides into a clone that differentiates into plasma cells, which secrete specific antibodies, and memory cells. Cytokines also activate T-killer cells, which destroy infected body cells displaying the antigen. Because selection and cloning take days, the primary response is slow. Memory cells stay in the blood for years, so a second exposure to the same antigen triggers a secondary response that is faster and much larger: this is long-term immunity.
Press Next step to work through all eight steps. Notice that only one of the five T-helper cells and one of the five B-lymphocytes, the ones with red receptors, are selected. Watch for the yellow cytokines and the antibodies released by the plasma cells.
| Cell | What it does in the primary response |
|---|---|
| macrophage | engulfs the pathogen, digests it and places its antigens on its cell surface membrane: an antigen-presenting cell |
| T-helper cell | the cell with complementary receptors binds the presented antigen (clonal selection), divides by mitosis (clonal expansion) and releases cytokines |
| B-lymphocyte | the cell whose receptors (antibody molecules on its surface) fit the antigen binds it; cytokines stimulate it to divide by mitosis into a clone |
| plasma cell | a differentiated B cell with lots of rough ER, Golgi and mitochondria; secretes large amounts of one antibody, then dies within days |
| T-killer cell | activated by cytokines; binds to body cells displaying the antigen (virus-infected or cancer cells) and kills them, for example by making holes in their membranes |
| memory cells | long-lived B and T cells from the clones; remain in the blood after the infection |
B-lymphocytes mature in the bone marrow and T-lymphocytes mature in the thymus. B cells give the humoral response (antibodies in body fluids); T cells give the cell-mediated response.
Clonal selection is not the lymphocyte "making" a receptor to fit the antigen. The lymphocyte with a complementary receptor already exists before the infection; the antigen only selects it.
Press First infection and watch the graph, then press Same pathogen again. Compare when antibody production starts, how high it peaks and how long it lasts.
| Primary response | Secondary response | |
|---|---|---|
| delay before antibodies appear | several days (about 7 in the sim) | very short (about 2 in the sim) |
| peak antibody concentration | low (10 units in the sim) | much higher (100 units, ten times more) |
| how long antibodies last | falls quickly | stays high for longer |
| symptoms | the person usually becomes ill | the pathogen is destroyed before symptoms appear |
Long-term immunity is due to memory cells, not to antibodies staying in the blood. Antibodies are broken down within weeks; memory cells remain.
Four quick checks. Each correct answer earns XP and records this skill on your profile.
In step 2 of the primary response sim, what does the macrophage do with the pathogen's antigens?
In the sim, why is only one of the five T-helper cells selected?
In the sim, what do the yellow dots released by the T-helper clones represent?
On the secondary response graph in the sim, how does the second peak compare with the first?
Unlocks once the four checks above are done. Worth more XP, written to AS Paper 1 and Paper 2 standard.
Which cells secrete antibodies?
What is meant by clonal expansion?
A person is infected with the same strain of virus for a second time and does not become ill. What is the best explanation?
What is the role of T-killer cells in the primary immune response?
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