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Questions on the specific immune response
Antigens and the distinction between self and non-self; the cellular response with T-helper and T-killer cells, clonal selection and clonal expansion; the humoral response with B cells, plasma cells and memory cells; primary against secondary responses; and HIV as the infection that attacks the T-helper cells that co-ordinate the response.
17 original questions · 61 marks · the specific immune response notes · Pathogens, disease and immunity
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Describe the sequence of events from a pathogen entering the body to antibody appearing in the blood plasma.
Mark scheme
- B1 the pathogen is engulfed by a phagocyte, which hydrolyses it and presents its antigens on its own cell-surface membrane
- B1 a T-helper cell with a complementary receptor binds to the presented antigen and is activated, which is clonal selection, and divides by mitosis
- B1 the same antigen binds to the surface antibody of the B cell that fits it, and that B cell takes the antigen in, processes it and presents it
- B1 an activated T-helper cell binds to the presenting B cell and stimulates it to divide by mitosis, which is clonal expansion
- B1 the clone differentiates into plasma cells, which secrete antibody, and memory cells, which secrete nothing
Compare the cellular response with the humoral response, referring to the lymphocytes involved, to what each of those lymphocytes recognises, and to what finally destroys or disables the pathogen.
Mark scheme
- B1 both begin with clonal selection, the antigen binding the lymphocytes whose receptors are complementary to it, and both continue with clonal expansion by mitosis and leave memory cells behind
- B1 the cellular response is carried out by T lymphocytes, which are made in the bone marrow but mature in the thymus, whereas the humoral response is carried out by B lymphocytes, which mature in the bone marrow itself
- B1 a T cell responds only to antigen presented on a cell surface, whereas a B cell binds free antigen in blood and lymph using the antibody in its own cell-surface membrane, although it still needs an activated T-helper cell before it divides
- B1 the cellular response acts on the body's own cells, a T-killer cell binding an infected cell and releasing perforin so that it dies, whereas the humoral response acts outside cells, plasma cells secreting soluble antibody that agglutinates pathogens and marks them for phagocytosis
- A1 so the cellular response is the one that can reach a virus already inside a host cell and the humoral response the one that deals with bacteria and toxins in the plasma, but they run at the same time and share the T-helper cell, so neither is a separate system
Explain why detectable antibody appears about eight days after a first exposure to an antigen but only about two days after a second exposure to the same antigen.
Mark scheme
- B1 on the first exposure the antigen must first be presented by a phagocyte, and the few lymphocytes with a complementary receptor must be selected out of millions
- B1 those selected cells must then divide repeatedly by mitosis before enough exist to matter, and only then do plasma cells appear and begin secreting
- B1 on the second exposure, memory cells specific to that antigen are already circulating in thousands rather than ones, so selection has already happened
- B1 the memory cells divide rapidly straight into plasma cells, so antibody is secreted in quantity within about two days
Explain why an untreated HIV infection eventually leaves a person unable to deal with infections that an intact immune system would handle easily.
Mark scheme
- B1 HIV infects T-helper cells specifically, using the CD4 protein on their surface as its way in, and replicates inside them
- B1 infected T-helper cells are killed, by the virus replicating inside them or by T-killer cells destroying them, so over years the number of T-helper cells falls
- B1 B cells are no longer properly activated, so few plasma cells are produced and little antibody is secreted
- B1 T-killer cells are no longer activated, so infected body cells are not destroyed; the infections that follow are what constitute AIDS
A virus is replicating inside the cells lining a person's airways. Suggest how T-killer cells limit the infection, and suggest why antibody alone would not be enough.
Mark scheme
- B1 a cell containing a replicating virus displays viral antigens on its own cell-surface membrane
- B1 a T-killer cell with a complementary receptor binds to that cell and releases perforin, which makes pores in the cell-surface membrane
- B1 granzymes enter through the pores and trigger apoptosis, so the infected cell dies before the virus inside it can finish replicating
- B1 antibody binds antigens outside cells, so it cannot reach virus particles already inside a host cell; only destroying the infected cell removes them
Lymphocytes carrying receptors that fit the body's own antigens are produced before birth but do not survive. Explain how this leaves a person tolerant of their own cells, and explain what has gone wrong in an autoimmune disease such as type 1 diabetes.
Mark scheme
- B1 lymphocytes are produced with an enormous variety of receptor shapes, generated before any antigen has been met, so some of them inevitably fit antigens carried on the body's own cells
- B1 during foetal development and shortly after birth, any lymphocyte whose receptor binds a self antigen dies or is suppressed, so the population left responds only to shapes the body does not contain
- B1 self antigens are therefore not treated as foreign and no response is mounted against them, while non-self antigens on a pathogen, a transplanted organ or a cell with altered surface proteins still provoke one
- B1 in an autoimmune disease, that screening has failed, so a lymphocyte specific to a self antigen has survived and been activated and the response is directed at the body's own tissue; in type 1 diabetes the cells that secrete insulin are destroyed
The table describes four cells taken from a person who is fighting an infection. Identify each of the four cells, and identify which of them are acting as antigen-presenting cells.
Cell What has been observed about it W has engulfed a pathogen, hydrolysed it with enzymes from a lysosome, and now carries fragments of the pathogen's antigens on its own cell-surface membrane X is a body cell in which a virus is replicating, and it carries viral antigens on its own cell-surface membrane Y carries thousands of copies of one antibody in its cell-surface membrane, and has taken in, processed and displayed the antigen those antibodies fit Z secretes about two thousand antibody molecules a second and displays no antigen on its surface Mark scheme
- A1 W is a phagocyte, and it is an antigen-presenting cell; its presentation is what begins the specific response
- A1 X is an infected body cell, which is presenting antigen too, and a T-killer cell with a complementary receptor binds to it
- A1 Y is a B cell, and it is also an antigen-presenting cell, presenting to an activated T-helper cell whose binding is what stimulates it to divide
- A1 Z is a plasma cell, which secretes antibody and presents nothing, so it is not an antigen-presenting cell
A new drug blocks the surface protein an activated T-helper cell uses to signal to a B cell that is presenting antigen, without affecting T-helper cell numbers or phagocytosis. Suggest how this would affect a person's ability to produce antibody against a new infection.
Mark scheme
- B1 phagocytosis and antigen presentation by phagocytes would be unaffected, since neither depends on this protein
- B1 T-helper cells could still be activated by antigen presented by a phagocyte, since the drug does not affect antigen recognition
- B1 but T-helper cells bound to a presenting B cell could no longer signal to it, so B cells would not receive the signal needed to divide
- A1 clonal expansion of B cells would be severely reduced, so few plasma cells and little antibody would be produced even though phagocytosis and T-helper cell activation are both normal
Describe the development of the cell-mediated immune response to a virus, including the role of cytokines.
Mark scheme
- B1 an antigen-presenting cell displays viral antigen on its cell-surface membrane
- B1 a T-helper cell with a complementary receptor binds, is selected and divides by mitosis
- B1 the activated T-helper cells release cytokines that stimulate T-killer cells with a complementary receptor to divide by mitosis
- B1 the T-killer cells bind to infected cells displaying the viral antigen and release perforin, so the infected cells die
T-helper cells and T-killer cells are separate lineages that are committed while they mature in the thymus. Explain why a T-helper cell cannot differentiate into a T-killer cell later in an infection.
Mark scheme
- B1 the two do different jobs: a T-helper cell releases cytokines that stimulate B cells, T-killer cells and phagocytes, whereas a T-killer cell destroys infected body cells itself
- B1 which job a T cell does is fixed during its maturation in the thymus, before it ever meets an antigen
- B1 when an antigen activates a T-helper cell, it divides by mitosis into a clone of genetically identical T-helper cells, so the response makes more T-helper cells and never T-killer cells
A plasma cell can secrete about 2000 antibody molecules a second. Calculate the number of antibody molecules one plasma cell secretes in 24 hours, giving your answer in standard form, and suggest one feature of the ultrastructure of a plasma cell that allows this rate of secretion.
Mark scheme
- M1 2000 × 60 × 60 × 24
- A1 1.7 × 108 antibody molecules (accept 1.73 × 108)
- B1 any one of: extensive rough endoplasmic reticulum, with many ribosomes, to make the antibody protein; a large Golgi apparatus to package it into vesicles; many mitochondria to supply ATP
A person vaccinated against hepatitis B as a baby is found, twenty years later, to have almost no antibody against the virus circulating in their blood, yet they remain protected against it. Suggest why.
Mark scheme
- B1 most plasma cells survive only a few days, so the concentration of antibody falls once the response to the vaccine is over
- B1 memory cells, unlike plasma cells, secrete no antibody but can persist for decades
- A1 on meeting hepatitis B antigen again, the memory cells would divide rapidly into plasma cells and mount a fast secondary response, so protection comes from the memory cells rather than from circulating antibody
Compare how a T cell recognises antigen with how a B cell recognises antigen.
Mark scheme
- B1 a T cell responds only to antigen presented on the surface of another cell, whereas a B cell can bind free antigen directly using the antibody in its own cell-surface membrane
- B1 despite binding free antigen, a B cell still needs an activated T-helper cell to bind to the antigen it then presents before it is fully activated and divides
- A1 so the two forms of recognition are not independent: a B cell's own recognition of antigen is not sufficient on its own for clonal expansion to proceed
Give three examples of things, other than a pathogen, that carry non-self antigens and so can provoke an immune response.
Mark scheme
- B1 a transplanted organ, which carries the donor's antigens on its cells
- B1 a cancer cell, which often displays abnormal surface proteins recognised as non-self
- B1 a toxin, which is a foreign molecule that can itself provoke antibodies without any cell being involved
Outline three things that cytokines released by an activated T-helper cell stimulate or activate.
Mark scheme
- B1 cytokines activate B cells that have presented the same antigen, triggering clonal expansion
- B1 cytokines activate T-killer (cytotoxic T) cells that have bound the same presented antigen
- B1 cytokines also stimulate phagocytes, making them engulf pathogens more actively
Explain the role of cytokines released by T-helper cells in the humoral immune response.
Mark scheme
- B1 a T-helper cell activated by antigen on an antigen-presenting cell binds to a B cell presenting the same antigen
- B1 it releases cytokines, such as interleukins, which bind to receptors on that B cell
- B1 the cytokines stimulate the B cell to divide by mitosis and the clone to differentiate into plasma cells, which secrete antibody, and memory cells
State what is meant by clonal selection and state what is meant by clonal expansion.
Mark scheme
- B1 clonal selection is the binding of an antigen to the lymphocytes whose receptors are complementary to it, activating those cells and no others
- B1 clonal expansion is the repeated division of each selected lymphocyte by mitosis, producing a large clone of genetically identical cells
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